The substance with the engram Cell phone as well as synaptic

Maximum and minimum water content was also determined. RESULTS Analyses of bark decorations and bark fissuring were not enough to explain the preference found for some tropical trees. In contrast, a positive relationship was found among water-storage capacity, bark porosity, and phorophyte preference. The host trees preferred by most orchids have bark with higher pore density and higher water retention after draining. CONCLUSIONS Unexpectedly, the phorophytes preferred by orchids are not those with more fissured bark but those with a higher ability to retain minimum water content after draining, which is a bark property positively correlated with higher pore density. Our data indicate that the bark microenvironment, determined by topology and water storage capacity, has a pivotal role in phorophyte specificity, a key factor that affects orchid diversity and distribution in the world. © 2020 Botanical Society of America.BACKGROUND AND PURPOSE High-fat diet (HFD)-induced obesity is accompanied by metabolic and neurochemical changes that have been associated with depression. Emerging studies indicate that palmitoylethanolamide (PEA) exerts metabolic effects and holds neuroprotective potential. However, studies on HFD exposure in mice which investigate the effects of PEA on monoamine system and synaptic plasticity are limited. EXPERIMENTAL APPROACH In C57Bl/6J male mice, obesity was established by HFD feeding for 12 weeks. Then, mice were treated with ultra-micronized PEA (30 mg·kg-1 daily p.o) or vehicle for 7 weeks along with HFD. Mice receiving chow diet and vehicle served as controls. Thereafter, depressive-, anhedonic-like behaviour and cognitive performance were measured. Monoamine analyses were performed on brain areas (nucleus accumbens, Nac; prefrontal cortex, PFC; hippocampus) and markers of synaptic plasticity and neurogenesis were evaluated in hippocampus. KEY RESULTS PEA limited depressive- and anhedonic-like behaviour, and cognitive deficits induced by HFD. PEA induced an increase in serotonin levels in PFC, and a reduction of dopaminergic and serotoninergic turnover in Nac and PFC, respectively. Moreover, PEA increased dopamine levels in the hippocampus and PFC. At molecular level, PEA restored brain-derived neurotrophic factor signaling pathway in hippocampus and PFC, indicating an improvement of synaptic plasticity. In particular, PEA counteracted the reduction of glutamatergic synaptic density induced by HFD in the stratum radiatum of the CA1 of the hippocampus, where it also exhibited neurogenesis promoting abilities. CONCLUSION AND IMPLICATIONS PEA may represent an adjuvant therapy to limit depressive-like behaviours and memory deficit, affecting monoamine homeostasis, synaptic plasticity, and neurogenesis. This article is protected by copyright. All rights reserved.Many hypotheses have been proposed to explain how a glutamate to valine substitution in sickle haemoglobin (HbS) can cause sickle cell disease (SCD). We propose and document a new mechanism in which elevated tyrosine phosphorylation of Band 3 initiates sequelae that cause vaso-occlusion and the symptoms of SCD. In this mechanism, denaturation of HbS and release of heme generate intracellular oxidants which cause inhibition of erythrocyte tyrosine phosphatases, thus permitting constitutive tyrosine phosphorylation of Band 3. This phosphorylation in turn induces dissociation of the spectrin-actin cytoskeleton from the membrane, leading to membrane weakening, discharge of membrane-derived microparticles (which initiate the coagulation cascade) and release of cell-free HbS (which consumes nitric oxide) and activates the endothelium to express adhesion receptors). These processes promote vaso-occlusive events which cause SCD. We further show that inhibitors of Syk tyrosine kinase block Band 3 tyrosine phosphorylation, prevent release of cell-free Hb, inhibit discharge of membrane-derived microparticles, increase sickle cell deformability, reduce sickle cell adhesion to human endothelial cells, and enhance sickle cell flow through microcapillaries. In view of reports that imatinib (a Syk inhibitor) successfully treats symptoms of sickle cell disease, we suggest that Syk tyrosine kinase inhibitors warrant repurposing as potential treatments for SCD. © 2020 British Society for Haematology and John Wiley & Sons Ltd.Epstein-Barr virus (EBV) is a human herpesvirus spread in childhood by contact with saliva. In all populations, the great majority of people are infected by middle age. EBV can cause asymptomatic infection, nonspecific symptoms or, especially in adolescents and young adults, the infectious mononucleosis (IM), characterized by pharyngitis, lymphadenopathy, fatigue, and fever. Two main types of skin rashes, accounted as atypical exanthems, occur in patients with acute IM a faint erythematous maculopapular eruption of 24-48 hours duration (5-15% of the patients) or a pruritic maculopapular rash in almost all patients receiving ampicillin or amoxicillin. DuP-697 molecular weight Moreover EBV acute infection has been related to other cutaneous manifestations, such as Gianotti-Crosti syndrome, unilateral laterothoracic exanthem (especially in children), and others. In this study, we reported a case of atypical exanthem with an erythematous-papulovesicular pattern in a 22-year-old female patient with IM and performed a review of the literature of the cutaneous and mucosal eruptions occurring during EBV acute infections. © 2020 the International Society of Dermatology.BACKGROUND AND PURPOSE Febrile seizures (FS), the most common seizures in childhood and often accompanied by later epileptogenesis, are not well controlled. Inflammatory processes have been implicated in the pathophysiology of epilepsy. However, whether the caspase-1 (Casp1) is involved in FS generation and potential to be a target for the treatment of FS is still unclear. EXPERIMENTAL APPROACH By using pharmacology and gene intervention methods, we tested the role of caspase-1 in FS generation. Then, based on structural virtual screening against the active pocket of caspase-1, we were aimed to find druggable and safe small-molecular antagonists targeting caspase-1 and test their therapeutic potential for FS. KEY RESULTS Here we show that caspase-1 is essential for FS generation. The level of cleaved caspase-1 increases prior to FS onset. Caspase-1-/- mice were resistant to FS and showed lower neuronal excitability than wild-type littermates. Conversely, overexpression of caspase-1 using in utero electroporation increased neuronal excitability and enhanced susceptibility to FS.