Capture and Separation, the First Step toward Circular Economy; a Regenerable, Bio-Based, Polymerized, Ionic Liquid Membranes

Air can be considered as a source of CO2, with concentrations of approximately 408 ppm reported in 2018 and predicted levels expected to reach 600−1550 ppm in 2030. Direct air capture (DAC) from the atmosphere is considered as a CO2 separation technology that can be realized and a source of CO2 exploitable as building block for utilization. The use of solid amines for CO2 adsorption following a two-steps process: the adsorption of CO2 from the direct air and the separation of CO2 from the sorbent. The separation of CO2 from amines is relatively easier than from strong liquid bases as it requires less energy due to the weaker bonds between CO2 and the solid sorbent. The benefit of the DAC technology is that it can be implemented anywhere because of the fast mixing of CO2 in the air. However this technique rely on the preparation of amine sorbed on solid inorganic substrate such as silica substrate and even if durable are quite difficult to regenerate once spent. Our substrate is based on polymerized ionic liquid that use as functional amino acid anions as active sorbent. Ionic liquids (ILs) are organic salts that melts below 100°C been studied as innovative material for CO2 capture. Polymerized ionic liquids (PILs) merge ILs and macromolecules peculiarities resulting in a novel class of material that features high tunability and ionic exchange ability as well as easier handling, processability typical of polymer. PILs have been studied for gas separation and demonstrated, higher CO2 loading than common ILs, as well as faster absorption/desorption rate. However, despite the chemical absorption of CO2 in ILs is a well-established concept divided as capture by chemisorption or by physisorption in PILs the majority of the studies focus on material without CO2 reactive species and no explicit reference to chemical nor physical sorption materials. Different PILs with amino acid anions were developed and tested for CO2 absorption in solid phase. The research on PILs aimed to explore different AA anions as well as different polymeric structures. Ionic exchange procedures were tuned depending on the solubility property of the starting PIL with several AA. All synthetic procedures aimed to avoid toxic and hazardou chemicals. Obtained PILs were identified and were tested for CO2 and water absorption and desorption

Imprese familiari e non familiari a confronto: il talent management.

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Development of a digital escape room to raise awareness of the effects of climate change on human health

Non peer reviewe

Theatre is a valid add-on therapeutic intervention for emotional rehabilitation of parkinson's disease patients

Conventional medical treatments of Parkinson's disease (PD) are effective on motor disturbances but may have little impact on nonmotor symptoms, especially psychiatric ones. Thus, even when motor symptomatology improves, patients might experience deterioration in their quality of life. We have shown that 3 years of active theatre is a valid complementary intervention for PD as it significantly improves the well-being of patients in comparison to patients undergoing conventional physiotherapy. Our aim was to replicate these findings while improving the efficacy of the treatment. We ran a single-blinded pilot study lasting 15 months on 24 subjects with moderate idiopathic PD. 12 were assigned to a theatre program in which patients underwent "emotional" training. The other 12 underwent group physiotherapy. Patients were evaluated at the beginning and at the end of their treatments, using a battery of eight clinical and five neuropsychological scales. We found that the emotional theatre training improved the emotional well-being of patients, whereas physiotherapy did not. Interestingly, neither of the groups showed improvements in either motor symptoms or cognitive abilities tested by the neuropsychological battery. We confirmed that theatre therapy might be helpful in improving emotional well-being in PD

Phenobarbital for neonatal seizures:response rate and predictors of refractoriness

Background : Phenobarbital is the first-line choice for neonatal seizures treatment, despite a response rate of approximately 45%. Failure to respond to acute anticonvulsants is associated with poor neurodevelopmental outcome, but knowledge on predictors of refractoriness is limited. Objective : To quantify response rate to phenobarbital and to establish variables predictive of its lack of efficacy. Methods : We retrospectively evaluated newborns with electrographically confirmed neonatal seizures admitted between January 1999 and December 2012 to the neonatal intensive care unit of Parma University Hospital (Italy), excluding neonates with status epilepticus. Response was categorized as complete (cessation of clinical and electrographic seizures after phenobarbital administration), partial (reduction but not cessation of electrographic seizures with the first bolus, response to the second bolus), or absent (no response after the second bolus). Multivariate analysis was used to identify independent predictors of refractoriness. Results : Out of 91 newborns receiving phenobarbital, 57 (62.6%) responded completely, 15 (16.5%) partially, and 19 (20.9%) did not respond. Seizure type (p = 0.02), background electroencephalogram (EEG; p ≤ 0.005), and neurologic examination (p ≤ 0.005) correlated with response to phenobarbital. However, EEG (p ≤ 0.02) and seizure type (p ≤ 0.001) were the only independent predictors. Conclusion : Our results suggest a prominent role of neurophysiological variables (background EEG and electrographic-only seizure type) in predicting the absence of response to phenobarbital in high-risk newborns

Distinctive Roles of Canonical and Noncanonical Wnt Signaling in Human Embryonic Cardiomyocyte Development

Open Access funded by British Heart Foundation Under a Creative Commons license Acknowledgments Our thanks go to Gioia Polidori Francisco for training and discussions, Kate Watt and Yvonne Turnbull for technical and laboratory managerial support, Kadri Oras and Laura Ferguson for experimental support, Po-Lin So and Bruce Conklin (Gladstone Institutes) for providing their unpublished protocols, and Yukio Nakamura for discussion. This research is supported by the British Heart Foundation (PG/12/75/29851) and the Institute of Medical Sciences. A.S.B. was supported by the British Heart Foundation (FS/12/37/29516).Peer reviewedPublisher PD

RhoA controls Wnt upregulation on microstructured titanium surfaces.

Rough topography enhances the activation of Wnt canonical signaling in vitro, and this mediates its effects on cell differentiation. However, the molecular mechanisms underlying topography-dependent control of Wnt signaling are still poorly understood. As the small GTPase RhoA controls cytoskeletal reorganization and actomyosin-induced tensional forces, we hypothesized that RhoA could affect the activation of Wnt signaling in cells on micropatterned titanium surfaces. G-LISA assay revealed that RhoA activation was higher in C2C12 cells on rough (SLA) surfaces under basal conditions than on smooth (Polished) titanium. Transfection with dominant negative RhoA decreased Wnt activation by normalized TCF-Luc activity on SLA, whilst transfection with constitutively active RhoA increased TCF-Luc activation on Polished titanium. One mM Myosin II inhibitor Blebbistatin increased RhoA activation but decreased Wnt activation on SLA surfaces, indicating that tension-generating structures are required for canonical Wnt modulation on titanium surfaces. Actin inhibitor Cytochalasin markedly enhanced RhoA and TCF-Luc activation on both surfaces and increased the expression of differentiation markers in murine osteoblastic MC3T3 cells. Taken together, these data show that RhoA is upregulated in cells on rough surfaces and it affects the activation of Wnt canonical signaling through Myosin II modulation

Plexin-D1/Semaphorin 3E pathway may contribute to dysregulation of vascular tone control and defective angiogenesis in systemic sclerosis

INTRODUCTION: The vascular and nervous systems have several anatomic and molecular mechanism similarities. Emerging evidence suggests that proteins involved in transmitting axonal guidance cues, including members of class III semaphorin (Sema3) family, play a critical role in blood vessel guidance during physiological and pathological vascular development. Sema3E is a natural antiangiogenic molecule that causes filopodial retraction in endothelial cells, inhibiting cell adhesion by disrupting integrin-mediated adhesive structures. The aim of the present study was to investigate whether in systemic sclerosis (SSc) Plexin-D1/Sema3E axis could be involved in the dysregulation of vascular tone control and angiogenesis. METHODS: Sema3E levels were measured by quantitative colorimetric sandwich ELISA in serum samples from 48 SSc patients, 45 subjects with primary Raynaud's phenomenon (pRP) and 48 age-matched and sex-matched healthy controls. Immunofluorescence staining on skin sections from 14 SSc patients and 12 healthy subjects was performed to evaluate Sema3E and Plexin-D1 expression. Western blotting was used to assess Plexin-D1/Sema3E axis in human SSc and healthy dermal microvascular endothelial cells (SSc-MVECs and H-MVECs, respectively) at basal condition and after stimulation with recombinant human vascular endothelial growth factor (VEGF), SSc and healthy sera. Capillary morphogenesis on Matrigel was performed on H-MVECs treated with healthy, pRP or SSc sera in the presence of Sema3E and Plexin-D1 soluble peptides. RESULTS: Serum Sema3E levels were significantly higher both in pRP subjects and SSc patients than in controls. In SSc, Sema3E levels were significantly increased in patients with early nailfold videocapillaroscopy (NVC) pattern compared to active/late patterns and pRP, and in patients without digital ulcers versus those with ulcers. In SSc skin, Sema3E expression was strongly increased in the microvascular endothelium. Cultured SSc-MVECs showed higher levels of phosphorylated Plexin-D1 and Sema3E expression than H-MVECs, and stimulation with SSc sera increased phosphorylated Plexin-D1 and Sema3E in H-MVECs. The addition of Sema3E-binding Plexin-D1 soluble peptide significantly attenuated the antiangiogenic effect of SSc sera on H-MVECs. CONCLUSIONS: Our findings suggest that Plexin-D1/Sema3E axis is triggered in SSc endothelium and may have a role in the dysregulation of angiogenesis and vascular tone control by inducing neuro-vascular mechanism alterations clinically evident in particular in the early disease phases

Pax9 and Gbx2 interact in the pharyngeal endoderm to control cardiovascular development.

The correct formation of the aortic arch arteries depends on a coordinated and regulated gene expression profile within the tissues of the pharyngeal arches. Perturbation of the gene regulatory networks in these tissues results in congenital heart defects affecting the arch arteries and the outflow tract of the heart. Aberrant development of these structures leads to interruption of the aortic arch and double outlet right ventricle, abnormalities that are a leading cause of morbidity in 22q11 Deletion Syndrome (DS) patients. We have recently shown that Pax9 functionally interacts with the 22q11DS gene Tbx1 in the pharyngeal endoderm for 4th pharyngeal arch artery morphogenesis, with double heterozygous mice dying at birth with interrupted aortic arch. Mice lacking Pax9 die perinatally with complex cardiovascular defects and in this study we sought to validate further potential genetic interacting partners of Pax9, focussing on Gbx2 which is down-regulated in the pharyngeal endoderm of Pax9-null embryos. Here, we describe the Gbx2-null cardiovascular phenotype and demonstrate a genetic interaction between Gbx2 and Pax9 in the pharyngeal endoderm during cardiovascular development