This study aimed to examine the direct and indirect effects of hope on health-related quality of life (HRQoL) via anxiety of children/adolescents with cancer. We proposed to test if the mediation model was moderated by the child/adolescent's treatment status. The participants were 211 children/adolescents diagnosed with cancer, divided into two clinical groups according to treatment status: 97 patients on-treatment and 114 off-treatment. Self-reported questionnaires measured the youths' hope, anxiety, and HRQoL perceptions. The results revealed that children/adolescents on- and off-treatment only differed in levels of HRQoL, with a more compromised HRQoL found for the on-treatment group. Hope was positively associated with HRQoL, directly and indirectly via anxiety reduction. Moreover, only the association between anxiety and HRQoL was moderated by clinical group, revealing stronger associations for on-treatment patients. Findings highlight the importance of hope as a decisive resource in pediatric cancer adaptation, which may be strategically targeted in psycho-oncological interventions.
SummaryForkhead box P3 (FoxP3)+ regulatory T cells (Tregs) are functionally deficient in systemic lupus erythematosus (SLE), characterized by reduced surface CD25 [the interleukin (IL)‐2 receptor alpha chain]. Low‐dose IL‐2 therapy is a promising current approach to correct this defect. To elucidate the origins of the SLE Treg phenotype, we studied its role through developmentally defined regulatory T cell (Treg) subsets in 45 SLE patients, 103 SLE‐unaffected first‐degree relatives and 61 unrelated healthy control subjects, and genetic association with the CD25‐encoding IL2RA locus. We identified two separate, uncorrelated effects contributing to Treg CD25. (1) SLE patients and unaffected relatives remarkably shared CD25 reduction versus controls, particularly in the developmentally earliest CD4+FoxP3+CD45RO–CD31+ recent thymic emigrant Tregs. This first component effect influenced the proportions of circulating CD4+FoxP3highCD45RO+ activated Tregs. (2) In contrast, patients and unaffected relatives differed sharply in their activated Treg CD25 state: while relatives as control subjects up‐regulated CD25 strongly in these cells during differentiation from naive Tregs, SLE patients specifically failed to do so. This CD25 up‐regulation depended upon IL2RA genetic variation and was related functionally to the proliferation of activated Tregs, but not to their circulating numbers. Both effects were found related to T cell IL‐2 production. Our results point to (1) a heritable, intrathymic mechanism responsible for reduced CD25 on early Tregs and decreased activation capacity in an extended risk population, which can be compensated by (2) functionally independent CD25 up‐regulation upon peripheral Treg activation that is selectively deficient in patients. We expect that Treg‐directed therapies can be monitored more effectively when taking this distinction into account.
SARS-CoV-2 infections can induce kidney injury and glomerulopathy, with the most common pathology findings being acute tubular injury and collapsing glomerulopathy.Here we describe a rare case of membranous nephropathy in a man in his late 70s presented with nephrotic syndrome and rapidly progressive kidney dysfunction 1 month after SARS-CoV-2 infection. Phospholipase A2 receptor antibodies were positive. He was treated with rituximab, with proteinuria control. We review the cases reported in the literature.
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