Predictors of treatment change and engagement in cognitive-behavioral group therapy for depression.

Examined predictors of treatment response in 48 individuals (mean age 40.71 yrs) who presented for participation in a 10-session cognitive-behavioral group therapy program for depression. The majority of Ss carried a diagnosis of major depression and all were concurrently on at least 1 antidepressant medication. The therapeutic approach involved an integration of 2 empirically supported therapies: Beck\u27s cognitive therapy (A. T. Beck et al, 1979) and Lewinsohn\u27s Coping With Depression course (P. M. Lewinsohn et al, 1984). Ss completed the Burns Depression Checklist, the Dysfunctional Attitudes Scale (DAS), and the Burns Hopelessness Scale, a 5-item questionnaire which assesses the degree of optimism/pessimism an individual has regarding mood and symptom control. No significant differences were found on pretreatment dysfunctional attitudes or depressive symptomatology between individuals who dropped out of treatment and treatment completers. However, pretreatment hopelessness scores were significantly higher in dropouts than in individuals who completed treatment. Increased pessimism about symptom control was also related to fewer reductions in DAS scores throughout treatment among completers and to poorer overall treatment response. (PsycINFO Database Record (c) 2017 APA, all rights reserved

Introduction to the Special Issue: Cognitive Mechanisms of Change in the Treatment of Depression

Depression is a highly debilitating and recurrent mental health condition. Efforts to understand the mechanisms of cognitive change in the treatment of depression are important to optimize psychotherapy outcome and to prevent relapse and recurrence. The articles in this special issue examine cognitive change in cognitive behavioral therapy by incorporating clinical samples and clinical settings, utilizing empirically supported assessment instruments and protocolized psychotherapy techniques, and employing methodologies and statistical strategies designed to address questions related to cognitive mechanisms in treatment outcome. These articles examine the role of cognitive processing, structure, and content over the course of cognitive therapy for depression and evaluate the impact of positive and negative events on treatment outcomes

How long do mood induction procedure (MIP) primes really last? Implications for cognitive vulnerability research.

BACKGROUND: Mood Induction Procedures (MIPs) are used widely in research on cognitive vulnerability to depression. Although empirical evidence supports certain MIPs as effective, little research has evaluated whether MIP-induced sad moods are sufficiently persistent. This study aimed to determine (1) how long an MIP-induced mood lasts according to commonly used operational definitions and (2) whether these findings vary according to the type of MIP used. METHODS: Four-hundred-and-one undergraduate students were randomly assigned to one of three commonly used sad MIPs (music, memory, music+memory) or to one of three matched neutral MIPs. Mood was repeatedly measured immediately prior to and following the MIP. RESULTS: Results did not support the widely held belief that commonly used MIPs induce a sufficient and persistent sad mood. The memory-related MIPs induced the most persistent sad mood. Based on the majority of operational definitions, however, induced mood effects did not last longer than 4 min, regardless of MIP type. LIMITATIONS: Future studies should examine additional factors that may have affected the trajectories observed in the current study (e.g., task completed in between mood measurements) and in vulnerable (e.g., past-depressed) populations. CONCLUSIONS: This study constitutes an important first step in validating the use of MIPs in cognitive vulnerability research and provides researchers with important information on future study designs. More important, the study raises doubt about the validity of various conclusions drawn from some MIP studies and calls into question the theoretical conceptualizations of depression that are based on potentially biased results and a possibly incomplete literature

Cognitive Structure and Processing During Cognitive Behavioral Therapy vs. Pharmacotherapy for Depression

Background: Evidence has converged to suggest that cognitive processing and content covary with depression severity, whereas indices of cognitive structure exhibit greater stability and promise as markers of vulnerability for depression. The objective of the current study was to investigate the temporal dynamics and causal role of cognitive structure and processing in treatment for depression. Method: A total of 104 patients with major depressive disorder were randomized to receive cognitive behavioral therapy (CBT; n = 54) or pharmacotherapy (n = 50). Patients completed the Hamilton Depression Rating Scale (HAM-D), Beck Depression Inventory-II (BDI-II), Psychological Distance Scaling Task (PDST), Redundancy Card-Sorting Task (RCST), and Self-Referent Encoding Task (SRET) before, during, and after treatment. Results: Most cognitive indices exhibited change over treatment to a similar degree across both treatments. Evidence for the mediating role of cognition was limited, and not specific to CBT. Discussion: Results suggest that both cognitive structure and processing may be amenable to change, by both CBT and pharmacotherapy. The role of cognitive structure in the course of depression may require qualification

Cognitive change in cognitive-behavioural therapy

BACKGROUND: Although cognitive-behavioural therapy (CBT) is a well-established treatment for adult depression, its efficacy and efficiency may be enhanced by better understanding its mechanism(s) of action. According to the theoretical model of CBT, symptom improvement occurs via reductions in maladaptive cognition. However, previous research has not established clear evidence for this cognitive mediation model. METHODS: The present study investigated the cognitive mediation model of CBT in the context of a randomized controlled trial of CBT v. antidepressant medication (ADM) for adult depression. Participants with major depressive disorder were randomized to receive 16 weeks of CBT (n = 54) or ADM (n = 50). Depression symptoms and three candidate cognitive mediators (dysfunctional attitudes, cognitive distortions and negative automatic thoughts) were assessed at week 0 (pre-treatment), week 4, week 8 and week 16 (post-treatment). Longitudinal associations between cognition and depression symptoms, and mediation of treatment outcome, were evaluated in structural equation models. RESULTS: Both CBT and ADM produced significant reductions in maladaptive cognition and depression symptoms. Cognitive content and depression symptoms were moderately correlated within measurement waves, but cross-lagged associations between the variables and indirect (i.e. mediated) treatment effects were non-significant. CONCLUSIONS: The results provide support for concurrent relationships between cognitive and symptom change, but not the longitudinal relationships hypothesized by the cognitive mediation model. Results may be indicative of an incongruence between the timing of measurement and the dynamics of cognitive and symptom change

The role of outcome expectancy in therapeutic change across psychotherapy versus pharmacotherapy for depression.

BACKGROUND: Patient outcome expectancy - the belief that treatment will lead to an improvement in symptoms - is linked to favourable therapeutic outcomes in major depressive disorder (MDD). The present study extends this literature by investigating the temporal dynamics of expectancy, and by exploring whether expectancy during treatment is linked to differential outcomes across treatment modalities, for both optimistic versus pessimistic expectancy. METHODS: A total of 104 patients with MDD were randomized to receive either cognitive behavioral therapy (CBT) or pharmacotherapy for 16 weeks. Outcome expectancy was measured throughout treatment using the Depression Change Expectancy Scale (DCES). Depression severity was measured using both the Hamilton Depression Rating Scale and Beck Depression Inventory-II. RESULTS: Latent growth curve models supported improvement in expectancy across both treatments. Cross-lagged panel models revealed that both higher optimistic and lower pessimistic expectancy at mid-treatment predicted greater treatment response in pharmacotherapy. For CBT, the associative patterns between expectancy and depression differed as a function of expectancy type; higher optimistic expectancy at pre-treatment and lower pessimistic expectancy at mid-treatment predicted greater treatment response. LIMITATIONS: The sample size limited statistical power and the complexity of models that could be explored. CONCLUSIONS: Results suggest that outcome expectancy improved during treatment for depression. Whether outcome expectancy represents a specific mechanism for the reduction of depression warrants further investigation

The stress-responsive Hsp90 chaperone is required for the production of the genotoxin colibactin and the siderophore yersiniabactin by Escherichia coli

The genotoxin colibactin synthesized by Escherichia coli is a secondary metabolite belonging to the chemical family of hybrid polyketide/non-ribosomal peptide compounds. It is produced by a complex biosynthetic assembly line encoded by the pks pathogenicity island. The presence of this large cluster of genes in the E. coli genome is invariably associated with the High-Pathogenicity Island, encoding the siderophore yersiniabactin that belongs to the same chemical family as colibactin. The E. coli heat shock protein HtpG (Hsp90Ec) is the bacterial homolog of the eukaryotic molecular chaperone Hsp90 involved in the protection of cellular proteins against a variety of environmental stresses. In contrast to the eukaryotic Hsp90, the functions and client proteins of Hsp90Ec are poorly known. Here, we demonstrated that production of colibactin and yersiniabactin is abolished in the absence of Hsp90Ec We further characterized an interplay between the Hsp90Ec molecular chaperone and the ClpQ protease involved in colibactin and yersiniabactin synthesis. Finally, we demonstrated that Hsp90Ec is required for the full in vivo virulence of extraintestinal pathogenic E. coli This is the first report highlighting the role of heat shock protein Hps90Ec in the production of two secondary metabolites involved in E. coli virulence

Functional activities of the Tsh protein from avian pathogenic Escherichia coli (APEC) strains

The temperature-sensitive hemagglutinin (Tsh) expressed by strains of avian pathogenic Escherichia (E.) coli (APEC) has both agglutinin and protease activities. Tsh is synthesized as a 140 kDa precursor protein, whose processing results in a 106 kDa passenger domain (Tshs) and a 33 kDa β-domain (Tshβ). In this study, both recombinant Tsh (rTsh) and supernatants from APEC, which contain Tshs (106 kDa), caused proteolysis of chicken tracheal mucin. Both rTsh (140 kDa) and pellets from wild-type APEC, which contain Tshβ (33 kDa), agglutinated chicken erythrocytes. On Western blots, the anti-rTsh antibody recognized the rTsh and 106 kDa proteins in recombinant E. coli BL21/pET 101-Tsh and in the supernatants from APEC grown at either 37℃ or 42℃. Anti-rTsh also recognized a 33 kDa protein in the pellets from APEC13 cultures grown in either Luria-Bertani agar, colonization factor antigen agar, or mucin agar at either 26℃, 37℃, or 42℃, and in the extracts of outer membrane proteins of APEC. The 106 kDa protein was more evident when the bacteria were grown at 37℃ in mucin agar, and it was not detected when the bacteria were grown at 26℃ in any of the culture media used in this study. Chicken anti-Tsh serum inhibited hemagglutinating and mucinolytic activities of strain APEC13 and recombinant E. coli BL21/pET101-Tsh. This work suggests that the mucinolytic activity of Tsh might be important for the colonization of the avian tracheal mucous environment by APEC

Infections with Avian Pathogenic and Fecal Escherichia coli Strains Display Similar Lung Histopathology and Macrophage Apoptosis

The purpose of this study was to compare histopathological changes in the lungs of chickens infected with avian pathogenic (APEC) and avian fecal (Afecal) Escherichia coli strains, and to analyze how the interaction of the bacteria with avian macrophages relates to the outcome of the infection. Chickens were infected intratracheally with three APEC strains, MT78, IMT5155, and UEL17, and one non-pathogenic Afecal strain, IMT5104. The pathogenicity of the strains was assessed by isolating bacteria from lungs, kidneys, and spleens at 24 h post-infection (p.i.). Lungs were examined for histopathological changes at 12, 18, and 24 h p.i. Serial lung sections were stained with hematoxylin and eosin (HE), terminal deoxynucleotidyl dUTP nick end labeling (TUNEL) for detection of apoptotic cells, and an anti-O2 antibody for detection of MT78 and IMT5155. UEL17 and IMT5104 did not cause systemic infections and the extents of lung colonization were two orders of magnitude lower than for the septicemic strains MT78 and IMT5155, yet all four strains caused the same extent of inflammation in the lungs. The inflammation was localized; there were some congested areas next to unaffected areas. Only the inflamed regions became labeled with anti-O2 antibody. TUNEL labeling revealed the presence of apoptotic cells at 12 h p.i in the inflamed regions only, and before any necrotic foci could be seen. The TUNEL-positive cells were very likely dying heterophils, as evidenced by the purulent inflammation. Some of the dying cells observed in avian lungs in situ may also be macrophages, since all four avian E. coli induced caspase 3/7 activation in monolayers of HD11 avian macrophages. In summary, both pathogenic and non-pathogenic fecal strains of avian E. coli produce focal infections in the avian lung, and these are accompanied by inflammation and cell death in the infected areas

A longitudinal twin and sibling study of the hopeless theory of depression in adolescence and young adulthood

Background Maladaptive cognitive biases such as negative attributional style and hopelessness have been implicated in the development and maintenance of depression. According to the hopelessness theory of depression, hopelessness mediates the association between attributional style and depression. The aetiological processes underpinning this influential theory remain unknown. The current study investigated genetic and environmental influences on hopelessness and its concurrent and longitudinal associations with attributional style and depression across adolescence and emerging adulthood. Furthermore, given high co-morbidity between depression and anxiety, the study investigated whether these maladaptive cognitions constitute transdiagnostic cognitive content common to both internalizing symptoms. Method A total of 2619 twins/siblings reported attributional style (mean age 15 and 17 years), hopelessness (mean age 17 years), and depression and anxiety symptoms (mean age 17 and 20 years). Results Partial correlations revealed that attributional style and hopelessness were uniquely associated with depression but not anxiety symptoms. Hopelessness partially mediated the relationship between attributional style and depression. Hopelessness was moderately heritable (A = 0.37, 95% confidence interval 0.28–0.47), with remaining variance accounted for by non-shared environmental influences. Independent pathway models indicated that a set of common genetic influences largely accounted for the association between attributional style, hopelessness and depression symptoms, both concurrently and across development. Conclusions The results provide novel evidence that associations between attributional style, hopelessness and depression symptoms are largely due to shared genetic liability, suggesting developmentally stable biological pathways underpinning the hopelessness theory of depression. Both attributional style and hopelessness constituted unique cognitive content in depression. The results inform molecular genetics research and cognitive treatment approaches