Compassion focused therapy: Exploring the effectiveness with a transdiagnostic group and potential processes of change.

OBJECTIVES: This study aimed to examine the effectiveness of a compassion focused therapy (CFT) group with a transdiagnostic population, as compared to treatment as usual (TAU). A secondary aim was to explore the potential processes of change within the treatment. DESIGN: A non-randomized control trial was used. METHOD: Fifty-eight participants who engaged in group CFT were compared to 29 participants receiving TAU. Group CFT consisted of 14 sessions twice weekly for 5 weeks and once weekly for 4 weeks. Participants completed measures of psychopathology, shame, self-criticism, fears of self-compassion, and social safeness, at pre-treatment, post-treatment, and 2-month follow-up. Potential processes of change were examined using correlations and regression analysis. RESULTS: Significantly greater improvements were found for levels of psychopathology, fears of self-compassion and social safeness for CFT, compared to TAU. Additionally, analyses showed improvements in shame and self-criticism within the CFT group but not the TAU group. All improvements were maintained at 2-month follow-up. Improvements in psychopathology were predicted by changes in self-criticism and fears of self-compassion. CONCLUSION: Compassion focused therapy appears to be an effective group intervention for a range of mental health difficulties. The positive impact of the CFT model with a transdiagnostic group emphasizes the value of addressing underlying psychological process, rather than symptoms alone. PRACTITIONER POINTS: Compassion focused therapy is a multimodal therapy designed to target high levels of shame and self-criticism. Compassion focused therapy has been shown previously to have positive results within a range of diagnostic-specific populations. While there is an emerging research base, limited studies assessing effectiveness with transdiagnostic populations have been published. CFT was shown to have a significant effect in reducing levels of psychopathology, compared to TAU. A number of potential processes of change were identified: Changes in psychopathology were significantly correlated with changes in self-criticism and fears of self-compassion.

Analysis of Gender Differences in Knowledge of Stroke Warning Signs.

BACKGROUND: The impact of gender on knowledge of stroke warning signs and preparedness is poorly understood, and gender-specific factors associated with poor knowledge of stroke warning signs have not been identified. METHODS: This was a cross-sectional study of 132,604 participants in the 2009 Behavioral Risk Factor Surveillance System Survey, a national telephone survey. Adults aged 18 years or older who lived in one of 19 states that administered an optional stroke module asking them to correctly identify stroke symptoms and the correct action to take were included. The primary outcome was a low score (≤ 4 of 7) on the Stroke Symptoms Knowledge Scale (SSKS). Logistic regression was performed for the overall sample and then stratified by gender, with adjustments made for age, race, Hispanic ethnicity, income, and whether respondents had a primary doctor (PMD). Data were weighted as recommended by the Centers for Disease Control. RESULTS: In all, 51.7% of the weighted sample was women. Less women than men had low scores on the SSKS (21% versus 25%, P < .001). After adjusting for age, race, ethnicity, income, and PMD, men had higher odds of having low scores (adjusted odds ratio, 1.36; 95% confidence interval, 1.28-1.45). After stratifying by gender, Hispanic ethnicity, and age younger than 35 years predicted low scores on the scale in women but not in men. CONCLUSIONS: Female gender is associated with better knowledge of stroke warning signs, but a gender-specific approach identified Hispanic women, young women, and black participants as subgroups at risk for having poor knowledge, suggesting the need for targeted stroke education to increase stroke preparedness in these groups.

Identification of Racial Inequities in Access to Specialized Inpatient Heart Failure Care at an Academic Medical Center.

BACKGROUND: Racial inequities for patients with heart failure (HF) have been widely documented. HF patients who receive cardiology care during a hospital admission have better outcomes. It is unknown whether there are differences in admission to a cardiology or general medicine service by race. This study examined the relationship between race and admission service, and its effect on 30-day readmission and mortality Methods: We performed a retrospective cohort study from September 2008 to November 2017 at a single large urban academic referral center of all patients self-referred to the emergency department and admitted to either the cardiology or general medicine service with a principal diagnosis of HF, who self-identified as white, black, or Latinx. We used multivariable generalized estimating equation models to assess the relationship between race and admission to the cardiology service. We used Cox regression to assess the association between race, admission service, and 30-day readmission and mortality. RESULTS: Among 1967 unique patients (66.7% white, 23.6% black, and 9.7% Latinx), black and Latinx patients had lower rates of admission to the cardiology service than white patients (adjusted rate ratio, 0.91; 95% CI, 0.84-0.98, for black; adjusted rate ratio, 0.83; 95% CI, 0.72-0.97 for Latinx). Female sex and age >75 years were also independently associated with lower rates of admission to the cardiology service. Admission to the cardiology service was independently associated with decreased readmission within 30 days, independent of race. CONCLUSIONS: Black and Latinx patients were less likely to be admitted to cardiology for HF care. This inequity may, in part, drive racial inequities in HF outcomes.

MMASS: an optimized array-based method for assessing CpG island methylation.

We describe an optimized microarray method for identifying genome-wide CpG island methylation called microarray-based methylation assessment of single samples (MMASS) which directly compares methylated to unmethylated sequences within a single sample. To improve previous methods we used bioinformatic analysis to predict an optimized combination of methylation-sensitive enzymes that had the highest utility for CpG-island probes and different methods to produce unmethylated representations of test DNA for more sensitive detection of differential methylation by hybridization. Subtraction or methylation-dependent digestion with McrBC was used with optimized (MMASS-v2) or previously described (MMASS-v1, MMASS-sub) methylation-sensitive enzyme combinations and compared with a published McrBC method. Comparison was performed using DNA from the cell line HCT116. We show that the distribution of methylation microarray data is inherently skewed and requires exogenous spiked controls for normalization and that analysis of digestion of methylated and unmethylated control sequences together with linear fit models of replicate data showed superior statistical power for the MMASS-v2 method. Comparison with previous methylation data for HCT116 and validation of CpG islands from PXMP4, SFRP2, DCC, RARB and TSEN2 confirmed the accuracy of MMASS-v2 results. The MMASS-v2 method offers improved sensitivity and statistical power for high-throughput microarray identification of differential methylation.

Trf1 is not required for proliferation or functional telomere maintenance in chicken DT40 cells.

The telomere end-protection complex prevents the ends of linear eukaryotic chromosomes from degradation or inappropriate DNA repair. The homodimeric double-stranded DNA-binding protein, Trf1, is a component of this complex and is essential for mouse embryonic development. To define the requirement for Trf1 in somatic cells, we deleted Trf1 in chicken DT40 cells by gene targeting. Trf1-deficient cells proliferated as rapidly as control cells and showed telomeric localization of Trf2, Rap1, and Pot1. Telomeric G-strand overhang lengths were increased in late-passage Trf1-deficient cells, although telomere lengths were unaffected by Trf1 deficiency, as determined by denaturing Southern and quantitative FISH analysis. Although we observed some clonal variation in terminal telomere fragment lengths, this did not correlate with cellular Trf1 levels. Trf1 was not required for telomere seeding, indicating that de novo telomere formation can proceed without Trf1. The Pin2 isoform and a novel exon 4, 5-deleted isoform localized to telomeres in Trf1-deficient cells. Trf1-deficient cells were sensitive to DNA damage induced by ionizing radiation. Our data demonstrate that chicken DT40 B cells do not require Trf1 for functional telomere structure and suggest that Trf1 may have additional, nontelomeric roles involved in maintaining genome stability.