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      Sleep Quality Following Hematopoietic Stem Cell Transplantation: Longitudinal Trajectories and Biobehavioral Correlates

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          Abstract

          The present study examined changes in sleep quality following hematopoietic stem cell transplantation (HSCT) and investigated associations with biobehavioral factors. Individuals undergoing HSCT for hematologic malignancies (N=228) completed measures of sleep quality and psychological symptoms pre-transplant and 1, 3, 6, and 12 months post-transplant. Circulating inflammatory cytokines (IL-6, TNF-α) were also assessed. Sleep quality was poorest at one month post-transplant, improving and remaining relatively stable after 3 months post-transplant. However, approximately half of participants continued to experience significant sleep disturbance at 6 and 12 months post-transplant. Mixed-effects linear regression models indicated that depression and anxiety were associated with poorer sleep quality, while psychological well-being was associated with better sleep. Higher circulating levels of IL-6 were also linked with poorer sleep. Subject-level fixed effects models demonstrated that among individual participants, changes in depression, anxiety, and psychological well-being were associated with corresponding changes in sleep after covarying for the effects of time since transplant. Sleep disturbance was most severe when depression and anxiety were greatest, and psychological well-being was lowest. Findings indicate that sleep disturbance is a persistent problem during the year following HSCT. Patients experiencing depression or anxiety and those with elevated inflammation may be at particular risk for poor sleep.

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          Diagnostic and statistical manual of mental disorders.

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            Neuroendocrine-immune mechanisms of behavioral comorbidities in patients with cancer.

            Patients with cancer experience a host of behavioral alterations that include depression, fatigue, sleep disturbances, and cognitive dysfunction. These behavioral comorbidities are apparent throughout the process of diagnosis and treatment for cancer and can persist well into the survivorship period. There is a rich literature describing potential consequences of behavioral comorbidities in patients with cancer including impaired quality of life, reduced treatment adherence, and increased disease-related morbidity and mortality. Medical complications of cancer and its treatment such as anemia, thyroid dysfunction, and the neurotoxicity of cancer chemotherapeutic agents account in part for these behavioral changes. Nevertheless, recent advances in the neurosciences and immunology/oncology have revealed novel insights into additional pathophysiologic mechanisms that may significantly contribute to the development of cancer-related behavioral changes. Special attention has been focused on immunologic processes, specifically activation of innate immune inflammatory responses and their regulation by neuroendocrine pathways, which, in turn, influence CNS functions including neurotransmitter metabolism, neuropeptide function, sleep-wake cycles, regional brain activity, and, ultimately, behavior. Further understanding of these immunologic influences on the brain provides a novel conceptual framework for integrating the wide spectrum of behavioral alterations that occur in cancer patients and may reveal a more focused array of translational targets for therapeutic interventions and future research. Such developments warrant complementary advances in identification of cancer patients at risk as well as those currently suffering, including an increased emphasis on the status of behavior as a "sixth vital sign" to be assessed in all cancer patients throughout their disease encounter.
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              Neural sensitivity to social rejection is associated with inflammatory responses to social stress.

              Although stress-induced increases in inflammation have been implicated in several major disorders, including cardiovascular disease and depression, the neurocognitive pathways that underlie inflammatory responses to stress remain largely unknown. To examine these processes, we recruited 124 healthy young adult participants to complete a laboratory-based social stressor while markers of inflammatory activity were obtained from oral fluids. A subset of participants (n = 31) later completed an fMRI session in which their neural responses to social rejection were assessed. As predicted, exposure to the laboratory-based social stressor was associated with significant increases in two markers of inflammatory activity, namely a soluble receptor for tumor necrosis factor-alpha (sTNFalphaRII) and interleukin-6 (IL-6). In the neuroimaging subsample, greater increases in sTNFalphaRII (but not IL-6) were associated with greater activity in the dorsal anterior cingulate cortex and anterior insula, brain regions that have previously been associated with processing rejection-related distress and negative affect. These data thus elucidate a neurocognitive pathway that may be involved in potentiated inflammatory responses to acute social stress. As such, they have implications for understanding how social stressors may promote susceptibility to diseases with an inflammatory component.
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                Author and article information

                Journal
                8702459
                2334
                Bone Marrow Transplant
                Bone Marrow Transplant.
                Bone marrow transplantation
                0268-3369
                1476-5365
                9 July 2014
                18 August 2014
                November 2014
                01 May 2015
                : 49
                : 11
                : 1405-1411
                Affiliations
                [1 ]Department of Health Outcomes & Behavior, Moffitt Cancer Center, Tampa, FL
                [2 ]Department of Psychology, University of Wisconsin-Madison, Madison, WI
                [3 ]Department of Medicine, Hematology/Oncology Division, University of Wisconsin-Madison, Madison, WI
                [4 ]Carbone Cancer Center, University of Wisconsin-Madison, Madison, WI
                [5 ]Department of Psychiatry, University of Wisconsin-Madison, Madison, WI
                [6 ]Center for Sleep Medicine and Research, University of Wisconsin-Madison, Madison, WI, United States
                [7 ]Department of Biostatistics & Medical Informatics, University of Wisconsin-Madison, Madison, WI
                Author notes
                Corresponding author for proof and reprints: Erin S. Costanzo, Department of Psychiatry, University of Wisconsin-Madison, 6001 Research Park Blvd, Madison, WI 53719, Phone: (608) 262-7515, ecostanzo@ 123456wisc.edu
                Article
                NIHMS608865
                10.1038/bmt.2014.179
                4221490
                25133898
                b9f22c8a-239e-4571-8e72-97f368a86687
                History
                Categories
                Article

                Transplantation
                cancer,hematopoietic stem cell transplantation,sleep,depression,anxiety,inflammation
                Transplantation
                cancer, hematopoietic stem cell transplantation, sleep, depression, anxiety, inflammation

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