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OBJECTIVE: Several nutritional strategies for the management of psoriasis are promising. Even if recent data support that nutrition may play a pivotal role in prevention and co-treatment and despite patient's concerns regarding the best nutritional habits, the consensus regarding the nutritional strategies to be adopted lacks in clinical settings. In this manuscript, the effects of several nutritional strategies for psoriasis patients such as hypocaloric diet, vitamin D, fish oil, selenium, and zinc supplementation were systematically reviewed. Randomized controlled trials (RCTs) on beneficial botanical oral supplements were also included in the analysis. MATERIALS AND METHODS: For each topic, a search was conducted in MEDLINE electronic databases for articles published in English between January 1, 1990 and September 2018. Two independent reviewers assessed and extracted the data. Only controlled clinical trials were selected. RESULTS: The evidence regarding the current nutritional strategies for psoriasis patients were summarized and translated into a global, comprehensible recommendation. CONCLUSIONS: Weight loss combined with a healthy lifestyle was shown to be very beneficial for patients with moderate to severe disease with a significant reduction of the Psoriasis Area and Severity Index (PASI) score. Currently, oral vitamin D supplementation for prevention or treatment of psoriasis in adults with normal vitamin D levels is not recommended; however, psoriasis patients with a deficit in plasma vitamin D levels are advised to complement with oral supplements to prevent psoriasis-related comorbidities. Instead of zinc, selenium, and omega 3 supplements have been proven beneficial for psoriasis patients. Among botanical species, Dunaliella bardawil (D. bardawil), Tripterygium wilfordii (T. wilfordii), Azadirachta indica (A. indica), Curcuma longa (C. longa), and HESA-A are the most beneficial. In conclusion, a close cooperation between nutritionists and dermatologists may be useful for the management of psoriasis.

Prismatic adaption (PA) has been proposed as a tool to induce neural plasticity and is used to help neglect rehabilitation. It leads to a recalibration of visuo-motor coordination during pointing as well as to after-effects on a number of sensorimotor and attention tasks, but whether these effects originate at a motor or attentional level remains a matter of debate. Our aim was to further characterise PA after-effects by using an approach that allows distinguishing between effects on attentional and motor processes. We recorded electroencephalography (EEG) in healthy human participants (9 females and 7 males) while performing a new double step, anticipatory attention/motor preparation paradigm before and after adaptation to rightward shifting prisms, with neutral lenses as a control. We then examined PA after-effects through changes in known oscillatory EEG signatures of spatial attention orienting and motor preparation in the alpha and beta frequency bands. Our results were twofold. First, we found PA to rightward shifting prisms to selectively affect EEG signatures of motor but not attentional processes. More specifically, PA modulated preparatory motor EEG activity over central electrodes in the right hemisphere, contralateral to the PA-induced, compensatory leftward shift in pointing movements. No effects were found on EEG signatures of spatial attention orienting over occipito-parietal sites. Second, we found the PA effect on preparatory motor EEG activity to dominate in the beta frequency band. We conclude that changes to intentional visuo-motor rather than attentional visuo-spatial processes underlie the PA after-effect of rightward deviating prisms in healthy participants.Significance StatementPrismatic adaptation (PA) has been proposed as a tool to induce neural plasticity in both healthy participants and patients, due to its after-effect impacting on a number of visuo-spatial and visuo-motor functions. However, the neural mechanisms underlying PA after-effects are poorly understood as only little neuroimaging evidence is available. Here, we examined for the first time the origin of PA after-effects studying oscillatory brain activity. Our results show a selective modulation of preparatory motor activity following PA in healthy participants but no effect on attention-related activity. This provides novel insight into the PA after-effect in the healthy brain and may help to inform interventions in neglect patients.

Multiple, action-based space representations are each based on the extent to which action is possible toward a specific sector of space, such as near/reachable and far/ unreachable. Studies on tool-use revealed how the boundaries between these representations are dynamic. Space is not only multidimensional and dynamic, but it is also known for interacting with other dimensions of magnitude, such as time. However, whether time operates on similar action-driven multiple representations and whether it can be modulated by tool-use is yet unknown. To address these issues, healthy participants performed a time bisection task in two spatial positions (near and far space) before and after an active tool-use training, which consisted of performing goal-directed actions holding a tool with their right hand (Experiment 1). Before training, perceived stimuli duration was influenced by their spatial position defined by action. Hence, a dissociation emerged between near/reachable and far/unreachable space. Strikingly, this dissociation disappeared after the active tool-use training since temporal stimuli were now perceived as nearer. The remapping was not found when a passive tool-training was executed (Experiment 2) or when the active tool-training was performed with participants’ left hand (Experiment 3). Moreover, no time remapping was observed following an equivalent active hand-training but without a tool (Experiment 4). Taken together, our findings reveal that time processing is based on action-driven multiple representations. The dynamic nature of these representations is demonstrated by the remapping of time, which is action- and effectordependent.

Using a twin coil transcranial magnetic stimulation (tc-TMS) approach we have previously demonstrated that facilitation may be detected in the primary motor cortex (M1) following stimulation over the ipsilateral caudal intraparietal sulcus (cIPS). Here we tested the interhemispheric interactions between the IPS and the contralateral motor cortex (M1). We found that conditioning the right cIPS facilitated contralateral M1 when the conditioning stimulus had an intensity of 90% resting motor threshold (RMT) but not at 70% or 110% RMT. Facilitation was maximal when the interstimulus interval (ISI) between cIPS and M1 was 6 or 12 ms. These facilitatory effects were mediated by interactions with specific groups of interneurons in the contralateral M1. In fact, short intracortical inhibition (SICI) was reduced following cIPS stimulation. Moreover, additional comparison of facilitation of responses evoked by anterior-posterior versus posterior-anterior stimulation of M1 suggested that facilitation was more effective on early I1/I2 circuits than on I3 circuits. In contrast to these effects, stimulation of anterior IPS (aIPS) at 90% RMT induced inhibition, instead of facilitation, of contralateral M1 at ISIs of 10-12 ms. Finally, we found similar facilitation between left cIPS and right M1 although the conditioning stimuli had to have a higher intensity compared with stimulation of right cIPS (110% instead of 90% RMT). These findings demonstrate that different subregions of the posterior parietal cortex (PPC) in humans exert both facilitatory and inhibitory effects towards the contralateral primary motor cortex. These corticocortical projections could contribute to a variety of motor tasks such as bilateral manual coordination, movement planning in space and grasping. © 2009 The Authors. Journal compilation © 2009 The Physiological Society.

Glycine GlyT2 transporters are localized on glycine-storing nerve endings. Their main function is to accumulate glycine to replenish synaptic vesicles. Glycine was reported to be costored with -aminobutyric acid (GABA) in cerebellar interneurons that may coexpress glycine and GABA transporters, and this is confirmed here by confocal microscopy analysis showing coexpression of GAT1 and GlyT2 transporters on microtubule-associated protein-2-positive synaptosomes. It was found that GABA uptake elicited glycine release from cerebellar nerve endings by various mechanisms. We investigated whether and by what mechanisms activation of glycine transporters could mediate release of GABA. Nerve endings purified from cerebellum were prelabeled with [H-3]GABA and exposed to glycine. Glycine stimulated [H-3]GABA release in a concentration-dependent manner. The glycine effect was insensitive to strychnine or to 5,7-dichlorokynurenate but it was abolished when GlyT2 transporters were blocked. About 20% of the evoked release was dependent on external Ca2+ entered by reversal of plasmalemmal Na+/Ca(2+)exchangers. A significant portion of the GlyT2-mediated release of [H-3]GABA (about 50% of the external Ca2+-independent release) occurred by reversal of GABA GAT1 transporters. Na+ ions, reaching the cytosol during glycine uptake through GlyT2, activated mitochondrial Na+/Ca2+ exchangers, causing an increase in cytosolic Ca2+, which in turn triggered a Ca2+-induced Ca2+ release process at inositoltrisphosphate receptors. Finally, the increased availability of Ca2+ in the cytosol allowed the opening of anion channels permeable to GABA. In conclusion, GlyT2 transporters not only take up glycine to replenish synaptic vesicles but can also mediate release of GABA by reversal of GAT1 and permeation through anion channels. (c) 2013 Wiley Periodicals, Inc.

Glycine GlyT2 transporters are localized on glycine-storing nerve endings. Their main function is to accumulate glycine to replenish synaptic vesicles. Glycine was reported to be costored with γ-aminobutyric acid (GABA) in cerebellar interneurons that may coexpress glycine and GABA transporters, and this is confirmed here by confocal microscopy analysis showing coexpression of GAT1 and GlyT2 transporters on microtubule-associated protein-2-positive synaptosomes. It was found that GABA uptake elicited glycine release from cerebellar nerve endings by various mechanisms. We investigated whether and by what mechanisms activation of glycine transporters could mediate release of GABA. Nerve endings purified from cerebellum were prelabeled with [3H]GABA and exposed to glycine. Glycine stimulated [3H]GABA release in a concentration-dependent manner. The glycine effect was insensitive to strychnine or to 5,7-dichlorokynurenate but it was abolished when GlyT2 transporters were blocked. About 20% of the evoked release was dependent on external Ca2+ entered by reversal of plasmalemmal Na+/Ca2+ exchangers. A significant portion of the GlyT2-mediated release of [3H]GABA (about 50% of the external Ca(2+)-independent release) occurred by reversal of GABA GAT1 transporters. Na+ ions, reaching the cytosol during glycine uptake through GlyT2, activated mitochondrial Na+/Ca2+ exchangers, causing an increase in cytosolic Ca2+, which in turn triggered a Ca(2+)-induced Ca2+ release process at inositoltrisphosphate receptors. Finally, the increased availability of Ca2+ in the cytosol allowed the opening of anion channels permeable to GABA. In conclusion, GlyT2 transporters not only take up glycine to replenish synaptic vesicles but can also mediate release of GABA by reversal of GAT1 and permeation through anion channels.

Polymyalgia rheumatica (PMR) is an inflammatory syndrome affecting older people whose prevalence has increased in recent years. The suppression of the hypothalamic-pituitary-adrenal axis (HPA) and ageing may contribute to the pathogenesis of PMR. Chronic stress (i.e. interpersonal, chronic infections etc.) in elderly people may represent a risk factor for the development of PMR. In fact, elderly represent per se a condition of endocrine senescence including adrenal hypofunction, in addition chronic stress represents a further harmful stimulus to seriously compromise endogenous glucocorticoid production. Synovitis and vasculitis characterize the majority of the patients. Serum cytokine and steroidal hormone patterns suggest that patients with PMR have an intensive inflammatory reaction. As a matter of fact, glucocorticoids represent the most useful temporary "replacement" treatment during the active phase of PMR. The use of modified-release glucocorticoids that might induce higher levels during the night (circadian rhythms as in physiological conditions), will represent another important approach to optimize PMR treatment and reduce the side effects. Combination therapy between glucocorticoids and inhibitors of pro-inflammatory cytokines should be tested in large studies and early cases of PMR.