False recalls, but not false recognitions, at the DRM paradigm are increased in subjects reporting insomnia symptoms: An online study.

BACKGROUND: In insomnia, poor sleep is accompanied by several cognitive impairments affecting prefrontal functioning that could affect source-monitoring processes and contribute to false memories production. By using a modified version of the Deese-Roediger-McDermott paradigm (DRM), we previously found that individuals suffering from insomnia produced more false memories than good sleepers adopting a free-recall task, especially for sleep-related stimuli. However, whether poor sleep affects false memory production in a task-dependent manner (i.e., free recall or recognition) remains unclear. METHODS: Through an online research method, we adopted the classical DRM paradigm to investigate the production of false recalls and false recognitions in 32 subjects referring insomnia symptoms (IN group) and 37 good sleepers (GS group), addressing also executive functioning and source monitoring ability in both groups. RESULTS: Compared to the GS group, the IN group produced more false memories (p = .002) and intrusions (p = .004) at the free recall task and showed a lower working memory index (p = .008). No between-groups differences emerged at the recognition task. Correlational analysis revealed significant associations between DRM performance, executive functioning and source monitoring (SM) variables. Moreover, false recalls were predicted by being in the presence of insomnia symptoms (p = .012) and intrusions by the number of correct responses to the Stroop task (p = .051) and SM task (p = .015), as well as by the presence of insomnia symptoms (p = .003). CONCLUSIONS: Our data show that the presence of insomnia symptoms can influence false memories production. Furthermore, the evidence that free recall is more affected than recognition suggests that poor sleep mainly affects performance at more cognitively demanding tasks. Finally, correlational and regression analyses support the hypothesis of a link between false memories production and both the presence of insomnia symptoms and executive functioning impairments.

Tuberculin skin test reactivity in Kawasaki disease.

A strongly positive tuberculin skin reaction (> 1.5 cm2) was observed during the acute phase of the illness in 11 children with Kawasaki disease (KD), but not in control pediatric patients with other febrile infections (41 patients) or diseases similar to KD (9 patients). The cutaneous sensitivity to intermediate strength [5 tuberculin units (TU)] purified protein derivative (PPD) inoculation had completely disappeared by the second monthly checkup. Peripheral blood T lymphocytes from KD subjects proliferated vigorously and produced significant amounts of IL-2 in response to the stimulation elicited by 0.05 TU/mL of PPD. In contrast, the proliferative response of, and IL-2 release by, control T cells was within background values. Mounting laboratory evidence suggests that heat shock proteins (HSP) may be involved in the pathogenesis of KD. Our clinical and experimental data may, therefore, have been due to immunologic cross-reactivity between mycobacterial derived HSP65 and its human homologue HPS63 (self P1 antigen). Despite the low number of patients investigated, our findings suggest that the tuberculin skin test and its in vitro correlates (T cell mitogenesis and IL-2 production) could provide simple and reliable diagnostic tools for identifying atypical forms of KD, or vice versa, in subjects not vaccinated against tuberculosis.

Soluble CD30 serum antigen in Kawasaki disease.

Very high levels of sCD30, a glycoprotein surface antigen expressed by T lymphocytes and other mononuclear cells of the immune system, were found in serum samples from 10 children with typical Kawasaki disease (KD), but not in blood specimens from a vast cohort of paediatric control subjects. These data strongly support an involvement of CD30 T cells in the immune processes which take place at the level of lymphoid organs during the acute phase of KD.

Soluble CD30 antigen in human colostrum.

It is now well established that the CD30 glycoprotein is a surface antigen expressed by activated T cells producing T-helper (Th)-2-type lymphokines. Mounting laboratory evidence, however, suggests that CD30 expression is not confined to a functionally restricted subset of T cells, but also identifies activated cells with a Th-1 and Th-0 pattern of cytokine secretion. CD30-bearing T lymphocytes release a soluble form of the molecule (sCD30), which can be detected both in vitro and in vivo. In the present study, very high levels of sCD30 were found in colostrum from 20 puerperal women, but not in autologous and heterologous (nonpregnant women) blood samples. These data strongly support an involvement of CD30+ T cells in the immune processes which take place at the level of the mammary gland during pregnancy and lactation. Passively transferred immune components such as immunoglobulins, cytokines, macrophages, natural killer cells, granulocytes and memory/activated T cells, all of which may help the baby to fight off infections, have been revealed in human breast milk. However, how Th-2-type cytokine-secreting T cells or other T-cell types help to endow the congenitally immunocompromised newborn infant with extrinsic immunological support remains an open question.