This study measured prevalence of depression and anxiety in SCD adults, and their effects on crisis and noncrisis pain, quality-of-life, opioid usage, and healthcare utilization. Methods: The Pain in Sickle Cell Epidemiology Study-is a prospective

cohort study in 308 SCD adults. Baseline variables included demographics, genotype, laboratory data, health-related quality-of-life, depression, and anxiety. Subjects completed daily diaries for up to 6 months, reporting sickle cell pain intensity, distress, interference, whether they were in a sickle cell crisis, as well as health care and opioid utilization. Results: Two hundred thirty-two subjects who completed at least 1 month of diaries were studied; 27.6% were depressed and 6.5% had any anxiety disorder. Depressed subjects had pain on significantly more days than

nondepressed subjects (mean pain days 71.1% versus 49.6%, p < .001). When in pain on noncrisis days, depressed JPH203 ic50 subjects had higher mean pain, distress from pain, and interference from pain. Both ZD1839 mouse depressed and anxious subjects bad poorer functioning on all eight SF-36 subscales, even after controlling for demographics, hemoglobin type, and pain. The anxious subjects had more pain, distress from pain, and interference from pain, both on noncrisis pain days and on crisis days, and used opioids more often. Conclusions: Depression and anxiety predicted more daily pain and poorer physical and mental quality-of-life in adults with SCD, and accounted for more of the variance in all domains

of quality-of-life than hemoglobin type.”
“Receptor editing is a key mechanism of B cell tolerance that modifies the B cell receptor (BcR) specificity of self-reactive lymphocytes. It acts through initiation of secondary immunoglobulin rearrangements, through generation of newly rearranged endogenous lambda chains that displace K chains, or through isotypic and allelic inclusion of dual BcRs (kappa(+)/lambda(+) FAD or kappa(+)/kappa(+) B cells). Mounting evidence indicates that receptor editing is either impaired or accelerated in patients suffering from rheumatic autoimmune diseases. Remarkably, both alterations can promote the pathogenesis of autoimmune disorders by favoring the uncontrolled emergence and/or persistence of autoreactivity. Whereas impaired secondary rearrangements might result in ineffective silencing of B cells, exacerbation of receptor editing can give rise to autoreactive receptors from clones that were initially devoid of autoreactivity.”
“Objective: Endothelial progenitor cells (EPCs) are capable of enhancing re-endothelialization and attenuating neointimal formation. However, inefficient homing limits the therapeutic efficacy of EPCs transplantation. CXCR4 plays a critical role in regulating EPCs homing. Here, we studied the effect of Foxc2 overexpression on CXCR4 expression and the homing capacity of EPCs as well as the EPCs-mediated therapeutic benefit after artery injury.