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There is ongoing debate regarding the relationship between clinical symptoms and cognition in schizophrenia spectrum disorders (SSD). The present study aimed to explore the potential relationships between symptoms, with an emphasis on negative symptoms, and social and non-social cognition.
Hierarchical cluster analysis with k-means optimisation was conducted to characterise clinical subgroups using the Scale for the Assessment of Negative Symptoms and Scale for the Assessment of Positive Symptoms in n = 130 SSD participants. Emergent clusters were compared on the MATRICS Consensus Cognitive Battery, which measures non-social cognition and emotion management as well as demographic and clinical variables. Spearman’s correlations were then used to investigate potential relationships between specific negative symptoms and emotion management and non-social cognition.
Four distinct clinical subgroups were identified: 1. high hallucinations, 2. mixed symptoms, 3. high negative symptoms, and 4. relatively asymptomatic. The high negative symptom subgroup was found to have significantly poorer emotion management than the high hallucination and relatively asymptomatic subgroups. No further differences between subgroups were observed. Correlation analyses revealed avolition-apathy and anhedonia-asociality were negatively correlated with emotion management, but not non-social cognition. Affective flattening and alogia were not associated with either emotion management or non-social cognition.
The present study identified associations between negative symptoms and emotion management within social cognition, but no domains of non-social cognition. This relationship may be specific to motivation, anhedonia and apathy, but not expressive deficits. This suggests that targeted interventions for social cognition may also result in parallel improvement in some specific negative symptoms.
The authors demonstrate that gold-binding peptides displayed on the outer membrane of Escherichia coli enhance bioelectrochemical charge transfer by binding gold nanoparticles. Microbial fuel cells were run with different gold-binding peptides displayed and with different nanoparticle sizes, and the results were correlated with transmission electron microscopy (TEM) imaging of nanoparticle binding. When a gold-binding peptide is displayed and 5 nm gold nanoparticles are present, up to 4× power generation over E. coli not displaying a gold-binding peptide is observed. While an enhanced current is observed using the previously published M6G9, the largest enhancement is observed when a new longer peptide named M9G18 is used.
Objectives: The Wisconsin Card Sorting Test (WCST) is a complex measure of executive function that is frequently employed to investigate the schizophrenia spectrum. The successful completion of the task requires the interaction of multiple intact executive processes, including attention, inhibition, cognitive flexibility, and concept formation. Considerable cognitive heterogeneity exists among the schizophrenia spectrum population, with substantive evidence to support the existence of distinct cognitive phenotypes. The within-group performance heterogeneity of individuals with schizophrenia spectrum disorder (SSD) on the WCST has yet to be investigated. A data-driven cluster analysis was performed to characterise WCST performance heterogeneity. Methods: Hierarchical cluster analysis with k-means optimisation was employed to identify homogenous subgroups in a sample of 210 schizophrenia spectrum participants. Emergent clusters were then compared to each other and a group of 194 healthy controls (HC) on WCST performance and demographic/clinical variables. Results: Three clusters emerged and were validated via altered design iterations. Clusters were deemed to reflect a relatively intact patient subgroup, a moderately impaired patient subgroup, and a severely impaired patient subgroup. Conclusions: Considerable within-group heterogeneity exists on the WCST. Identification of subgroups of patients who exhibit homogenous performance on measures of executive functioning may assist in optimising cognitive interventions. Previous associations found using the WCST among schizophrenia spectrum participants should be reappraised. (JINS, 2019, 25, 750–760)
Objectives: Antisaccade error rate has been proposed to be one of the most promising endophenotypes for schizophrenia. Increased error rate in patients has been associated with working memory, attention and other executive function impairments. The relationship between antisaccade error rate and other neuropsychological processes in patients compared to healthy controls has not been explored in depth. This study aimed to replicate the finding of heightened antisaccade error rate in patients and determine which cognitive processes were most strongly associated with antisaccade error rate in both patients and controls. In addition, the study investigated whether different antisaccade task paradigms engage different cognitive processes. Methods: One hundred and ninety-one participants (54 patients with schizophrenia/schizoaffective disorder and 137 controls) completed the antisaccade task, which included both gap and step task parameters. Neuropsychological measures were obtained using the MCCB and the Stroop task. Results: The current study replicated a pronounced antisaccade error rate deficit in patients. In patients, working memory variance was most significantly associated with antisaccade errors made during the step condition, while attentional processes were most associated with errors made during the gap condition. In controls, overall global cognitive performance was most associated with antisaccade rates for both gap and step conditions. Conclusions: The current study demonstrates that in schizophrenia patients, but not controls, elevated antisaccade error rate is associated with attention and working memory, but not with global cognitive impairment or psychopathological processes. Our novel findings demonstrate that the gap and step conditions of the antisaccade task engage different cognitive processes. (JINS, 2019, 25, 174–183)
Prior studies suggest that post-traumatic stress disorder (PTSD) is associated with elevated cardiovascular disease (CVD) risk, but effects of duration and remission of PTSD symptoms have rarely been evaluated.
We examined the association of time-updated PTSD symptom severity, remission and duration with incident CVD risk (552 confirmed myocardial infarctions or strokes) over 20 years in 49 859 women in the Nurses’ Health Study II. Among women who reported trauma on the Brief Trauma Questionnaire, PTSD symptoms, assessed by a screener, were classified by symptom severity and chronicity: (a) no symptoms, (b) 1–3 ongoing, (c) 4–5 ongoing, (d) 6–7 ongoing, (e) 1–3 remitted, (f) 4–7 remitted symptoms. Inverse probability weighting was used to estimate marginal structural logistic regression models, adjusting for time-varying and time-invariant confounders.
Compared with women with no trauma exposure, women with trauma/no PTSD [odds ratio (OR) 1.30, 95% confidence interval (CI) 1.03–1.65] and women with trauma/6–7 symptoms (OR 1.69, 95% CI 1.08–2.63) had elevated risk of CVD; women with remitted symptoms did not have elevated CVD risk. Among women exposed to trauma, every 5 additional years of PTSD symptomology was associated with 9% higher CVD incidence compared with women with trauma/no PTSD.
The findings suggest that alleviating PTSD symptoms shortly after onset may attenuate CVD risk.
Post-traumatic stress disorder (PTSD) has been declared ‘a life sentence’ based on evidence that the disorder leads to a host of physical health problems. Some of the strongest empirical research – in terms of methodology and findings – has shown that PTSD predicts higher risk of cardiometabolic diseases, specifically cardiovascular disease (CVD) and type 2 diabetes (T2D). Despite mounting evidence, PTSD is not currently acknowledged as a risk factor by cardiovascular or endocrinological medicine. This view is unlikely to change absent compelling evidence that PTSD causally contributes to cardiometabolic disease. This review suggests that with developments in methods for epidemiological research and the rapidly expanding knowledge of the behavioral and biological effects of PTSD the field is poised to provide more definitive answers to questions of causality. First, we discuss methods to improve causal inference using the observational data most often used in studies of PTSD and health, with particular reference to issues of temporality and confounding. Second, we consider recent work linking PTSD with specific behaviors and biological processes, and evaluate whether these may plausibly serve as mechanisms by which PTSD leads to cardiometabolic disease. Third, we evaluate how looking more comprehensively into the PTSD phenotype provides insight into whether specific aspects of PTSD phenomenology are particularly relevant to cardiometabolic disease. Finally, we discuss new areas of research that are feasible and could enhance understanding of the PTSD–cardiometabolic relationship, such as testing whether treatment of PTSD can halt or even reverse the cardiometabolic risk factors causally related to CVD and T2D.
Post-traumatic stress disorder (PTSD) has been linked to hypertension, but most research on PTSD and hypertension is cross-sectional, and potential mediators have not been clearly identified. Moreover, PTSD is twice as common in women as in men, but understanding of the PTSD-hypertension relationship in women is limited. We examined trauma exposure and PTSD symptoms in relation to incident hypertension over 22 years in 47 514 civilian women in the Nurses’ Health Study II.
We used proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for new-onset hypertension (N = 15 837).
PTSD symptoms assessed with a screen were modestly associated with incident hypertension in a dose-response fashion after adjusting for potential confounders. Compared to women with no trauma exposure, women with 6–7 PTSD symptoms had the highest risk of developing hypertension (HR 1.20, 95% CI 1.12–1.30), followed by women with 4–5 symptoms (HR 1.17, 95% CI 1.10–1.25), women with 1–3 symptoms (HR 1.12, 95% CI 1.06–1.18), and trauma-exposed women with no symptoms (HR 1.04, 95% CI 1.00–1.09). Findings were maintained, although attenuated, adjusting for hypertension-relevant medications, medical risk factors, and health behaviors. Higher body mass index and antidepressant use accounted for 30% and 21% of the PTSD symptom-hypertension association, respectively.
Screening for hypertension and reducing unhealthy lifestyle factors, particularly obesity, in women with PTSD may hold promise for offsetting cardiovascular risk.
We describe the cases of two children who both presented in infancy with recurrent severe pulmonary hypertensive crises. Exhaustive clinical work-up failed to identify an underlying aetiology. The patients had no clinical response to steroids, immunoglobulins, or pulmonary vasodilators. Post-mortem examination revealed extensive invasive pulmonary capillary haemangiomatosis. There was no evidence of pulmonary venous occlusive disease. Given the lethal nature of this condition, early consideration of referral to a lung transplant centre should be considered in selected patients.
We provide an introduction to enumerating and constructing invariants of group representations via character methods. The problem is contextualized via two case studies, arising from our recent work: entanglement invariants for characterizing the structure of state spaces for composite quantum systems; and Markov invariants, a robust alternative to parameter-estimation intensive methods of statistical inference in molecular phylogenetics.
Efficient emergency and disaster response is challenged by environmental conditions exceeding test reagent storage and operating specifications. We assessed the effectiveness of vial and foil packaging in preserving point-of-care (POC) glucose and lactate test strip performance in humid conditions.
Glucose and lactate test strips in both packaging were exposed to mean relative humidity of 97.0 ± 1.1% in an environmental chamber for up to 168 hours. At defined time points, stressed strips were removed and tested in pairs with unstressed strips using whole blood samples spiked to glucose concentrations of 60, 100, and 250 mg/dL (n = 20 paired measurements per level). A Wilcoxon signed rank test was used to compare stressed and unstressed test strip measurements.
Stressed glucose and lactate test strip measurements differed significantly from unstressed strips, and were inconsistent between experimental trials. Median glucose paired difference was as high as 12.5 mg/dL at the high glucose test concentration. Median lactate bias was −0.2 mmol/L. Stressed strips from vial (3) and foil (7) packaging failed to produce results.
Both packaging designs appeared to protect glucose and lactate test strips for at least 1 week of high humidity stress. Documented strip failures revealed the need for improved manufacturing process. (Disaster Med Public Health Preparedness. 2014;0:1–7)
Objective: To characterize the performance of glucose meter test strips using simulated dynamic temperature and humidity disaster conditions.
Methods: Glucose oxidase- and glucose dehydrogenase-based test strips were dynamically stressed for up to 680 hours using an environmental chamber to simulate conditions during Hurricane Katrina. Paired measurements vs control were obtained using 3 aqueous reagent levels for GMS1 and 2 for GMS2.
Results: Stress affected the performance of GMS1 at level 1 (P <. 01); and GMS2 at both levels (P <. 001), lowering GMS1 results but elevating GMS2 results. Glucose median-paired differences were elevated at both levels on GMS2 after 72 hours. Median-paired differences (stress minus control) were as much as −10 mg/dL (range, −65 to 33) at level 3 with GMS1, with errors as large as 21.9%. Glucose median-paired differences were as high as 5 mg/dL (range, −1 to 10) for level 1 on GMS2, with absolute errors up to 24.4%.
Conclusions: The duration of dynamic stress affected the performance of both GMS1 and GMS2 glucose test strips. Therefore, proper monitoring, handling, and storage of point-of-care (POC) reagents are needed to ensure their integrity and quality of actionable results, thereby minimizing treatment errors in emergency and disaster settings.
(Disaster Med Public Health Preparedness. 2012;6:232–240)
Bluetongue (BT) is a disease of ruminants caused by bluetongue virus (BTV), which is spread between its hosts by Culicoides midges. Vaccination is the most effective way to protect susceptible animals against BTV and was used reactively to control the recent northern European outbreak. To assess the consequences of using vaccination pre-emptively we used a stochastic, spatially explicit model to compare reactive and pre-emptive vaccination strategies against an incursion of BTV serotype 1 (BTV-1) into Great Britain. Both pre-emptive and reactive vaccination significantly reduced the number of affected farms and limited host morbidity and mortality. In addition, vaccinating prior to the introduction of disease reduced the probability of an outbreak occurring. Of the strategies simulated, widespread reactive vaccination resulted in the lowest levels of morbidity. The predicted effects of vaccination were found to be sensitive to vaccine efficacy but not to the choice of transmission kernel.
Beginning January 1, 2015, conventional cage housing for egg-laying hens is scheduled to be prohibited in California. We consider the economic implications of the new hen housing regulations on the California shell egg industry. Our data show that egg production is more costly using noncage systems than conventional cages. The main result of the new regulations will be a drastic reduction in the number of eggs produced in California, a large increase in egg shipments from out of state, little if any change in hen housing for eggs consumed in California, and little change in egg prices in California.