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Soy milk and pH-adjusted coconut water showed promising results as storage solutions for avulsed teeth, preserving the viability for up to 24 h.

Sleep is critical for hippocampus-dependent memory consolidation. However, the underlying mechanisms of synaptic plasticity are poorly understood. The central controversy is on whether long-term potentiation (LTP) takes a role during sleep and which would be its specific effect on memory. To address this question, we used immunohistochemistry to measure phosphorylation of Ca2+/calmodulin-dependent protein kinase II (pCaMKIIα) in the rat hippocampus immediately after specific sleep-wake states were interrupted. Control animals not exposed to novel objects during waking (WK) showed stable pCaMKIIα levels across the sleep-wake cycle, but animals exposed to novel objects showed a decrease during subsequent slow-wave sleep (SWS) followed by a rebound during rapid-eye-movement sleep (REM). The levels of pCaMKIIα during REM were proportional to cortical spindles near SWS/REM transitions. Based on these results, we modeled sleep-dependent LTP on a network of fully connected excitatory neurons fed with spikes recorded from the rat hippocampus across WK, SWS and REM. Sleep without LTP orderly rescaled synaptic weights to a narrow range of intermediate values. In contrast, LTP triggered near the SWS/REM transition led to marked swaps in synaptic weight ranking. To better understand the interaction between rescaling and restructuring during sleep, we implemented synaptic homeostasis and embossing in a detailed hippocampal-cortical model with both excitatory and inhibitory neurons. Synaptic homeostasis was implemented by weakening potentiation and strengthening depression, while synaptic embossing was simulated by evoking LTP on selected synapses. We observed that synaptic homeostasis facilitates controlled synaptic restructuring. The results imply a mechanism for a cognitive synergy between SWS and REM, and suggest that LTP at the SWS/REM transition critically influences the effect of sleep: Its lack determines synaptic homeostasis, its presence causes synaptic restructuring.

To evaluate the association between temporomandibular disorder (TMD) and anxiety, quality of sleep, and quality of life in nursing professionals at the Hospital de Clínicas de Uberlândia of the Universidade Federal de Uberlândia -HCU-UFU (Medical University Hospital of the Federal University of Uberlândia), four questionnaires were given to nursing professionals. The questionnaires were completed by 160 of these professionals. The Fonseca's questionnaire was used to evaluate the presence and severity of TMD, the IDATE was used to evaluate anxiety, the SAQ was used to evaluate quality of sleep, and the SF-36 was used to evaluate quality of life. Forty-one nurses (25.6%) reported having no TMD (Fonseca's questionnaire score ≤ 15), 66 (41.3%) had mild TMD (Fonseca's questionnaire score 20-40), 39 (24.4%) had moderate TMD (Fonseca's questionnaire score 45-65), and 14 (8.8%) had severe TMD (Fonseca's questionnaire score ≥ 70). According to Fonseca's questionnaire, the presence of TMD was associated with trait anxiety, but the TMD severity was associated with state anxiety classification (mild, moderate, severe). The SAQ score differed significantly from Fonseca classification. The Fonseca's questionnaire score correlated negatively with the score of each dimension of the SF-36 (r = -0.419 to -0.183). We conclude that TMD is common among nursing professionals; its presence was associated with trait anxiety, and its severity was associated with state anxiety. Hence, the presence of TMD may reduce quality of sleep and quality of life.