The aim of the present ex vivo study was to assess and compare coronal discoloration induced by four endodontic biomaterials used in regenerative endodontic procedures (REPs). Root resection was executed horizontally, 2 mm apical to the cementoenamel junction, in all fifty-four teeth. After accessing the pulp chamber, specimens were randomly divided in groups and filled with either saline solution or blood, followed by calcium silicate-based cements (CSCs) placement: ProRoot mineral trioxide aggregate (MTA) (Dentsply Sirona), Biodentine (Septodont), TotalFill BC (FKG), or pulp capping material (PCM) (Coltène). Color change (ΔE) was assessed using the L* a* b* system at five different timepoints (before and immediately after biomaterial application, 72 h, 7 days, and 6 months). The significance level for statistical analysis was set at p < 0.05. There are statistically significant differences regarding ΔE over time (p < 0.001). Statistical differences are found considering material (p < 0.001), treatment (p = 0.007), or both (p = 0.002). If solely the material or treatment is considered, regardless of time, statistically significant differences are detected (p < 0.001). After a six-month period of evaluation, blood exposure might be a critical factor in biomaterials’ color variation. Biodentine presents the lowest discoloration potential, followed by TotalFill and PCM, albeit without statistically significant differences. MTA exhibited the greatest color variation. The selection of biomaterial should consider the material’s discoloration potential.

Diphenyldibenzofulvene derivatives consisting of an aromatic tertbutyl-substituted fluorene stator and different rotors consisting of nonsubstituted phenyl groups (3,6-dtb-DPBF) and monomethyl-substituted (3,6-dtb-DPBFMe) and dimethyl-substituted [3,6-dtb-DPBF(Me) 2 ] forms have been synthesized and found to display aggregation-induced emission (AIE). The incremental number of substituents from 3,6-dtb-DPBF to the 3,6-dtb-DPBFMe and 3,6-dtb-DPBF-(Me) 2 derivatives promotes significant changes, from a good solvent (acetonitrile, MeCN), where it is very poorly emissive, to thin films or aggregates, in MeCN/ water mixtures, and a huge increment in fluorescence emission, which is found to be dependent on the water fraction, f w . The characteristics (size and distribution) of the aggregates were further corroborated with dynamic light scattering measurements. From time-resolved fluorescence experiments (TCSPC and FLIM), the increase in the contribution of the longer decay component is linked to the emission of the aggregate (AIE effect). To assist in the elucidation of the aggregation process at a molecular level, the data were complemented with computational studies [time-dependent density functional theory (TDDFT) and molecular dynamics (MD) simulations]. From MD, the octamer properly addresses the properties of the aggregate. As determined by the X-ray data, the crystal structure of a two-unit special disposition is identical to the geometry of the most stable structure obtained from MD and TDDFT calculations.

Adenosine receptors mainly control synaptic function, and excessive activation of adenosine receptors may worsen the onset of many neurological disorders. Accordingly, the regular intake of moderate doses of caffeine antagonizes adenosine receptors and affords robust neuroprotection. Although caffeine intake alters brain functional connectivity and multi-omics analyses indicate that caffeine intake modifies synaptic and metabolic processes, it is unclear how caffeine intake affects behavior, synaptic plasticity and its modulation by adenosine. We now report that male mice drinking caffeinated water (0.3 g/L) for 2 weeks were behaviorally indistinguishable (locomotion, mood, memory) from control mice (drinking water) and displayed superimposable synaptic plasticity (long-term potentiation) in different brain areas (hippocampus, prefrontal cortex, amygdala). Moreover, there was a general preservation of the efficiency of adenosine A1 and A2A receptors to control synaptic transmission and plasticity, although there was a tendency for lower levels of endogenous adenosine ensuring A1 receptor-mediated inhibition. In spite of similar behavioral and neurophysiological function, caffeine intake increased the energy charge and redox state of cortical synaptosomes. This increased metabolic competence likely involved a putative increase in the glycolytic rate in synapses and a prospective greater astrocyte–synapse lactate shuttling. It was concluded that caffeine intake does not trigger evident alterations of behavior or of synaptic plasticity but increases the metabolic competence of synapses, which might be related with the previously described better ability of animals consuming caffeine to cope with deleterious stimuli triggering brain dysfunction.

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Alzheimer’s disease (AD), which predominantly affects women, involves at its onset a metabolic deregulation associated with a synaptic failure. Here, we performed a behavioral, neurophysiological and neurochemical characterization of 9-month-old female APPswe/PS1dE9 (APP/PS1) mice as a model of early AD. These animals showed learning and memory deficits in the Morris water maze, increased thigmotaxis and anxiety-like behavior and showed signs of fear generalization. Long-term potentiation (LTP) was decreased in the prefrontal cortex (PFC), but not in the CA1 hippocampus or amygdala. This was associated with a decreased density of sirtuin-1 in cerebrocortical synaptosomes and a decreased density of sirtuin-1 and sestrin-2 in total cerebrocortical extracts, without alterations of sirtuin-3 levels or of synaptic markers (syntaxin, synaptophysin, SNAP25, PSD95). However, activation of sirtuin-1 did not affect or recover PFC-LTP deficit in APP/PS1 female mice; instead, inhibition of sirtuin-1 increased PFC-LTP magnitude. It is concluded that mood and memory dysfunction in 9-month-old female APP/PS1 mice is associated with a parallel decrease in synaptic plasticity and in synaptic sirtuin-1 levels in the prefrontal cortex, although sirtiun1 activation failed to restore abnormal cortical plasticity.

Steroidal 1-azadienes react with cyclic ketones to afford hexacyclic steroids via annulation reaction while the reaction with aldehydes gives pentacyclic steroids via hetero-Diels–Alder reactions.