Fatigue is a prominent quality of life concern among recipients of hematopoietic cell transplantation (HCT).

The present study investigated whether objectively measured sleep efficiency and sedentary behavior are related to greater reports of fatigue.

Eighty-two allogeneic HCT recipients who were 1-5 years post-transplant and returning for a follow-up visit participated (age M = 56, 52% female, 56% leukemia). They wore an actigraph assessing sleep efficiency and sedentary behavior for one week and completed an electronic log assessing fatigue each evening during the same period.

Twenty-six percent of patients reported clinically meaningful fatigue. GF120918 order On average, fatigue was mild (M = 2.5 on 0-10 scale, SD = 2.0), sleep was disturbed (sleep efficiency M = 78.9%, SD = 8.9), and patients spent the majority of time in sedentary (M = 55.4%, SD = 10.2) or light (M = 35.9%, SD = 8.6) activity. Multilevel model analysis of between-person differences indicated that patients who experienced less efficient sleep the previous evening provided greater evening reports of average fatigue, b = -0.06, 95% CI (-0.11, -0.01). Similarly, within-person analyses indicated that when patients experienced less efficient sleep the previous evening or were more sedentary as compared to their average, they provided greater evening reports of average fatigue, b = -0.02, 95% CI (-0.05, -0.004); b = 4.46, 95% CI (1.95, 6.97), respectively.

Findings demonstrate that poor sleep and daily sedentary behavior are related to evening reports of fatigue and should be considered modifiable targets for intervention.

Findings demonstrate that poor sleep and daily sedentary behavior are related to evening reports of fatigue and should be considered modifiable targets for intervention.

Psychological distress can influence cancer mortality through socioeconomic disadvantage, health-risk behaviors, or reduced access to care. These disadvantages can result in higher risks of cancer occurrence, a delayed cancer diagnosis, hamper adherence to treatment, and provoke inflammatory responses leading to cancer. Previous studies have linked psychological distress to cancer mortality. However, studies are lacking for the U.S. population.

This study examines the Kessler six-item psychological distress scale as a risk factor for U.S. cancer mortality using the pooled 1997-2014 data from the National Health Interview Survey (NHIS) linked to National Death Index (NDI) (N = 513,012). Cox proportional hazards regression was used to model survival time as a function of psychological distress and sociodemographic and behavioral covariates.

In Cox models with 18 years of mortality follow-up, the cancer mortality risk was 80% higher (hazard ratio [HR] = 1.80; 95% CI = 1.64, 1.97) controlling for age; 61% higher (HR = 1.61; 95% CI = 1.46, 1.76) in the SES-adjusted model, and 33% higher (HR = 1.33; 95% CI = 1.21, 1.46) in the fully-adjusted model among adults with serious psychological distress (SPD), compared with adults without psychological distress. Males, non-Hispanic Whites, and adults with incomes at or above 400% of the federal poverty level had greater cancer mortality risk associated with SPD. Using an 8 years of mortality follow-up, those with SPD had 108% increased adjusted risks of mortality from breast cancer.

Our study findings underscore the significance of addressing psychological well-being in the population as a strategy for reducing cancer mortality.

Our study findings underscore the significance of addressing psychological well-being in the population as a strategy for reducing cancer mortality.Germline genetic variants have been identified, which predispose individuals and families to develop melanoma. Tumor thickness is the strongest predictor of outcome for clinically localized primary melanoma patients. We sought to determine whether there is a heritable genetic contribution to variation in tumor thickness. If confirmed, this will justify the search for specific genetic variants influencing tumor thickness. To address this, we estimated the proportion of variation in tumor thickness attributable to genome-wide genetic variation (variant-based heritability) using unrelated patients with measured primary cutaneous melanoma thickness. As a secondary analysis, we conducted a genome-wide association study (GWAS) of tumor thickness. The analyses utilized 10 604 individuals with primary cutaneous melanoma drawn from nine GWAS datasets from eight cohorts recruited from the general population, primary care and melanoma treatment centers. Following quality control and filtering to unrelated individuals with study phenotypes, 8125 patients were used in the primary analysis to test whether tumor thickness is heritable. An expanded set of 8505 individuals (47.6% female) were analyzed for the secondary GWAS meta-analysis. Analyses were adjusted for participant age, sex, cohort and ancestry. We found that 26.6% (SE 11.9%, P = 0.0128) of variation in tumor thickness is attributable to genome-wide genetic variation. While requiring replication, a chromosome 11 locus was associated (P  less then  5 × 10-8) with tumor thickness. Our work indicates that sufficiently large datasets will enable the discovery of genetic variants associated with greater tumor thickness, and this will lead to the identification of host biological processes influencing melanoma growth and invasion.Spinal muscular atrophy (SMA) is a devastating childhood disease primarily affecting lower motoneurons in the spinal cord. SMA is caused by the loss of functional survival of motoneuron (SMN) protein, leading to structural and functional alterations of the cytoskeleton in motoneurons and other cells. Loss of SMN results in impairments of microtubule architecture, but the underlying mechanisms are not completely understood. In this study, we mechanistically analyzed the effects of SMN deficiency on microtubules, demonstrating a reduced stability together with a reduction in alpha tubulin detyrosination. This was caused by increased levels of microtubule-associated protein 1B and tubulin tyrosine ligase, resulting in mitochondrial mislocalization in SMA. Our findings suggest that altered tubulin post-translational modifications and microtubule-associated proteins are involved in the pathomechanisms of SMA, such as an impaired axonal transport of mitochondria.