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Metal–halide perovskites have gained extreme interest in the photovoltaic field with formamidinium lead iodide (FAPbI3) currently being one of the best‐performing materials for single‐junction solar cells. Despite the outstanding record efficiencies, there are still several major issues hindering the large‐scale fabrication of perovskite solar cells. The vulnerability to environmental agents along with the need of controlled atmosphere and crystallization aids for the perovskite film deposition represents the major roadblocks. This is particularly true for FAPbI3 for which the thermodynamically stable phase at room temperature is photovoltaically inactive δ‐phase. To address those challenges, herein, a camphorsulfonic‐salified chitosan is specifically designed with the aid of DTF calculations to strongly interact with the perovskite and, as a result, improve the morphology and optoelectronic quality of the FAPbI3. Thanks to the numerous interactions and then the modulation of the solution viscosity, FAPbI3 devices are fabricated by gravure printing deposition without either antisolvent bath or inclusion of methylammonium chloride (MACl) as additive. The gravure‐printed devices with the chitosan feature an enhanced efficiency and stability in air, retaining 80% of the original efficiency after 1200 h in ambient air without any encapsulation. [ABSTRACT FROM AUTHOR]

Aims: The 2021 European Society of Cardiology (ESC) screening recommendations for individuals carrying a pathogenic transthyretin amyloidosis variant (ATTRv) are based on expert opinion. We aimed to (i) determine the penetrance of ATTRv cardiomyopathy (ATTRv‐CM) at baseline; (ii) examine the value of serial evaluation; and (iii) establish the yield of first‐line diagnostic tests (i.e. electrocardiogram, echocardiogram, and laboratory tests) as per 2021 ESC position statement. Methods and results: We included 159 relatives (median age 55.6 [43.2–65.9] years, 52% male) at risk for ATTRv‐CM from 10 centres. The primary endpoint, ATTRv‐CM diagnosis, was defined as the presence of (i) cardiac tracer uptake in bone scintigraphy; or (ii) transthyretin‐positive cardiac biopsy. The secondary endpoint was a composite of heart failure (New York Heart Association class ≥II) and pacemaker‐requiring conduction disorders. At baseline, 40/159 (25%) relatives were diagnosed with ATTRv‐CM. Of those, 20 (50%) met the secondary endpoint. Indication to screen (≤10 years prior to predicted disease onset and absence of extracardiac amyloidosis) had an excellent negative predictive value (97%). Other pre‐screening predictors for ATTRv‐CM were infrequently identified variants and male sex. Importantly, 13% of relatives with ATTRv‐CM did not show any signs of cardiac involvement on first‐line diagnostic tests. The yield of serial evaluation (n = 41 relatives; follow‐up 3.1 [2.2–5.2] years) at 3‐year interval was 9.4%. Conclusions: Screening according to the 2021 ESC position statement performs well in daily clinical practice. Clinicians should adhere to repeating bone scintigraphy after 3 years, as progressing to ATTRv‐CM without signs of ATTRv‐CM on first‐line diagnostic tests or symptoms is common. [ABSTRACT FROM AUTHOR]

Background: SNCA p.V15A was reported in five families. In vitro models showed increased aggregation and seeding activity, mitochondrial damage, and apoptosis. Mutant flies had reduced flying ability and survival. Objectives: To clinically and functionally evaluate SNCA p.V15A in a large Italian family with Parkinson's disease (PD). Methods: Genetic diagnosis was reached through next‐generation sequencing. Pathogenicity was assessed by molecular dynamics simulation and biochemical studies on peripheral blood mononuclear cells (PBMCs). Results: Five siblings carried SNCA p.V15A; three developed bradykinetic‐rigid PD in their 50s with rapid motor progression and variable cognitive impairment. A fourth sibling had isolated mood disturbance, whereas the fifth was still unaffected at age 47. The mutant protein showed decreased stability and an unstable folded structure. Proband's PBMCs showed elevated total and phosphorylated α‐synuclein (α‐syn) levels and significantly reduced glucocerebrosidase activity. Conclusion: This study demonstrates accumulation of α‐synV15A in PBMCs and strengthens the link between α‐syn pathophysiology and glucocerebrosidase dysfunction. © 2024 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Optical antennas are nanostructures that introduce unprecedented possibilities for light–matter interaction at the nanoscale. An appropriately tailored plasmonic antenna can enhance the total radiative decay rate and modify the angular radiation pattern of a single‐quantum emitter through controlled near‐field coupling. Despite their ability to surpass the fundamental diffraction limit and confine the electromagnetic field to a tiny mode volume, fabricating 3D sharp scanning nanoscale plasmonic structures with desired aspect ratio is yet an ambitious goal. The fabrication of nanocones by gold evaporation on commercial atomic force microscopy probes followed by a focused ion beam milling technique is presented. The method is versatile and allows the fabrication of nanocones with desired dimensions around 100 nm along with an aspect ratio of ≈1. Their optical properties are studied and it is shown how the variation in the refractive index of the dielectric substrate affects the localized surface plasmon resonance of the nanocones, the decay rate enhancement, and the quantum yield of an emitter relevant for fluorescence/Raman scanning experiments. Theoretical studies using finite‐difference time‐domain calculations have guided the fabrication process and are consistent with experimental results. [ABSTRACT FROM AUTHOR]

Trilostane is a 3β‐hydroxysteroid dehydrogenase/Δ5‐4 isomerase inhibitor able to produce a manyfold increase in brain levels of various neurosteroids, including allopregnanolone. We previously found that treatment with trilostane can slow down epileptogenesis in the kainic acid (KA) model of temporal lobe epilepsy. It is unknown whether trilostane may have a similar effect on the progression of epilepsy severity, as observed in KA‐treated rats. Consequently, we investigated the effects of trilostane (50 mg/kg/day, 1 week) in epileptic rats, given 64 days after KA administration. Seizures were monitored by video‐electrocorticographic recordings before and during the treatment with trilostane or vehicle (sesame oil), and neurosteroid levels were measured in serum and cerebral tissue using liquid chromatography–electrospray tandem mass spectrometry after treatment. Pregnenolone sulfate, pregnenolone, progesterone, 5α‐dihydroprogesterone, and allopregnanolone peripheral levels were massively increased by trilostane. With the only exception of hippocampal pregnenolone sulfate, the other neurosteroids augmented in both the neocortex and hippocampus. Only pregnanolone levels were not upregulated by trilostane. As expected, a significant increase in the seizure occurrence was observed in rats receiving the vehicle, but not in the trilostane group. This suggests that the increased availability of neurosteroids produced a disease‐modifying effect in the brain of epileptic rats. [ABSTRACT FROM AUTHOR]

Neuropsychiatric disorders are anticipated to be a leading health concern in the near future, emphasizing an outstanding need for the development of new effective therapeutics to treat them. Stilbenes, with resveratrol attracting the most attention, are an example of multi‐target compounds with promising therapeutic potential for a broad array of neuropsychiatric and neurological conditions. This review is a comprehensive summary of the current state of research on stilbenes in several neuropsychiatric and neurological disorders such as depression, anxiety, schizophrenia, autism spectrum disorders, epilepsy, traumatic brain injury, and neurodegenerative disorders. We describe and discuss the results of both in vitro and in vivo studies. The majority of studies concentrate on resveratrol, with limited findings exploring other stilbenes such as pterostilbene, piceatannol, polydatin, tetrahydroxystilbene glucoside, or synthetic resveratrol derivatives. Overall, although extensive preclinical studies show the potential benefits of stilbenes in various central nervous system disorders, clinical evidence on their therapeutic efficacy is largely missing. [ABSTRACT FROM AUTHOR]

Background: Atopic dermatitis (AD) is characterized by Staphylococcus aureus (S. aureus) colonization. Longitudinal early life data delineating relationships of S. aureus colonization, barrier function, and AD outcomes are lacking. We define longitudinal S. aureus endotypes and AD pathogenesis in early life. Methods: We defined longitudinal S. aureus skin colonization phenotypes across two annual visits (non‐colonized: V1−V2−, early transient: V1+V2−, late‐onset: V1−V2+, persistent: V1+V2+) in the Mechanisms of Progression of Atopic Dermatitis to Asthma in Children cohort. We analyzed AD severity, sensitization, and skin barrier function across phenotypes, and performed mediation analyses between colonization and FLG expression. Results: Persistent S. aureus colonization was associated with increased SCORAD at V1 (33.5 vs. 19.0, p =.004) and V2 (40.1 vs.16.9, p <.001), and lower non‐lesional (NL) FLG at V2 (1.77 vs. 4.09, p =.029) compared to the non‐colonized phenotype, with early transient and late‐onset colonization as intermediate phenotypes. Children colonized at V2 demonstrated a decrease in NL‐FLG expression from V1 to V2 compared to those non‐colonized at V2 (p =.0012), who maintained expression. This effect remained significant even after adjusting for V1 colonization and SCORAD (p =.011). Conclusions: Our findings are the first to present longitudinal quantitative FLG expression and S. aureus skin colonization in early life and suggest that a decrease in NL‐FLG drives later colonization. Hence, therapies to maintain NL‐FLG expression may prevent S. aureus colonization. Further, a longitudinal AD endotype of persistent colonization is characterized by increased AD severity, sensitization, and decreasing NL‐FLG. [ABSTRACT FROM AUTHOR]

This article explores the role of thrombin and fibrinogen in atopic dermatitis (AD) in both human infants and mice models. The study found that children with AD under the age of 1 had increased thrombin generation and decreased time to peak thrombin compared to children without AD. Additionally, thrombin inhibition in mice resulted in decreased AD symptoms and fibrinogen deficiency in mice led to decreased disease development. These findings suggest that thrombin and fibrinogen may contribute to AD pathogenesis and could be potential targets for therapy. The study was funded by NIH and the American Academy of Allergy, Asthma, and Immunology Foundation. [Extracted from the article]

Machine learning models have become widespread in materials science research. An open‐access and community‐driven database containing over 40 000 perovskite photovoltaic devices has been recently published. This resource enables the application of predictive data‐driven models to correlate device structure with photovoltaic performance, whereas the literature usually focuses on specific device layers. Herein, the concept of device‐level performance prediction is explored using gradient‐boosted regression trees as the core algorithm and Shapley values analysis to interpret and rationalize the results. The main pitfalls and conceptual limitations of the approach are discussed and correlated with the database structure and dimension, by comparing the performance of different choices of descriptors and dataset size. Evidence suggests that the additional features introduced herein, in particular chemical descriptors of perovskite additives, can boost regression performance at a device level. A specific model is finally trained to predict the performance of unseen devices and tested on experimental data from the literature. This task is found to be particularly challenging, as the ability of the model to generalize to a new chemical space is limited by several factors, including the amount and the quality of available data. [ABSTRACT FROM AUTHOR]

This study assessed the influence of supplementing the rabbit semen extender with various concentrations of glutathione (GSH) and taurine at 24, 48, and 72 h postchilling at 5°C. Semen samples were collected from 20 New Zealand bucks, and ejaculates with standard color, motility (>85%), about 0.5 mL volume, and ∼400 × 106/mL concentration were used and diluted with extenders supplemented with 0.5, 1, and 2 mM of GSH and 1, 5, and 10 mM of taurine and chilled at 5°C. Nonsupplemented samples were used as a control. Sperm's progressive motility, acrosome reaction, and extracellular oxidative stress biomarkers such as MDA contents and GPx, SOD, and CAT concentrations and intracellular transcriptomic levels of SOD and CAT genes were assessed. GSH and taurine supplementation improved the sperm's kinetics by reducing cooling-associated stress, which was ascertained by lowering MDA concentration and increasing SOD, CAT, and GPx concentrations (P < 0.05). Increasing the levels of antioxidant enzymes in the extender was due to the increasing mRNA copies of the SOD and CAT genes (P < 0.05). Furthermore, GSH and taurine maintained the fructose levels in the extender and lowered the GPT levels, which implies sperm membrane stability is maintained through GSH and taurine supplementation. GSH and taurine supplementation to the extender had protective influences on the in vitro rabbit semen quality during chilled storage for up to 72 h, which were remarkable with increasing supplementation dose and cooling time at 5°C. [ABSTRACT FROM AUTHOR]

With the advances of diagnostic techniques, an ever-expanding spectrum of genes causing various dystonia syndromes is recognized.[1] Genetic syndromes combining dystonia and ataxia constitute a non-rare occurrence. Keywords: PMPCA gene variants; ataxia; dystonia; autosomal recessive transmission; phenotype EN PMPCA gene variants ataxia dystonia autosomal recessive transmission phenotype 1020 1023 4 06/20/23 20230601 NES 230601 Dystonia can be the manifestation of a plethora of genetic diseases. The PMPCA-related phenotype has been later expanded to include multisystem involvement consistent with mithocondriopathy[4] and occasional dystonia.[[5], [7]] In all these cases, ataxia was the presenting and the most severe motor disturbance. Ataxia, dystonia, autosomal recessive transmission, PMPCA gene variants, phenotype. [Extracted from the article]

Objective: Epileptogenesis after status epilepticus (SE) has a faster onset in rats treated to reduce brain levels of the anticonvulsant neurosteroid allopregnanolone with the 5α‐reductase inhibitor finasteride; however, it still has to be evaluated whether treatments aimed at increasing allopregnanolone levels could result in the opposite effect of delaying epileptogenesis. This possibility could be tested using the peripherally active inhibitor of 3β‐hydroxysteroid dehydrogenase/Δ5‐4 isomerase trilostane, which has been shown repeatedly to increase allopregnanolone levels in the brain. Methods: Trilostane (50 mg/kg) was administered subcutaneously once daily for up to six consecutive days, starting 10 min after intraperitoneal administration of kainic acid (15 mg/kg). Seizures were evaluated by video‐electrocorticographic recordings for 70 days maximum, and endogenous neurosteroid levels were assessed by liquid chromatography–electrospray tandem mass spectrometry. Immunohistochemical staining was performed to evaluate the presence of brain lesions. Results: Trilostane did not alter the latency of kainic acid‐induced SE onset or its overall duration. When compared to the vehicle‐treated group, rats receiving six daily trilostane injections presented a remarkable delay of the first spontaneous electrocorticographic seizure and subsequent tonic–clonic spontaneous recurrent seizures (SRSs). Conversely, rats treated with only the first trilostane injection during SE did not differ from vehicle‐treated rats in developing the SRSs. Notably, trilostane did not modify neuronal cell densities or the overall damage in the hippocampus. In comparison to the vehicle group, repeated administration of trilostane significantly decreased the activated microglia morphology in the subiculum. As expected, allopregnanolone and other neurosteroid levels were remarkably increased in the hippocampus and neocortex of rats treated for 6 days with trilostane, but pregnanolone was barely detectable. Neurosteroids returned to basal levels after a week of trilostane washout. Significance: Overall, these results suggest that trilostane led to a remarkable increase in allopregnanolone brain levels, which was associated with protracted effects on epileptogenesis. [ABSTRACT FROM AUTHOR]

Redispersible polymer powders (RDPPs), i.e., additives obtained from core–shell nanoparticles and commercialized in the form of a dry powder, find intensive application in the concrete industry. However, they are mainly produced from fossil resources. Therefore, the development of bio‐based RDPPs is important to reduce the carbon footprint of these additives. In this work, two types of core–shell nanoparticles with a high percentage of bio‐based content are synthesized and show to be good candidates as RDPPs. In the first case, up to 75% of bio‐based content is obtained by combining lauryl acrylate, derived from coconut and palm kernel oil, as main core material, with isobornyl methacrylate, coming from pine resin, exploited to create the outer harder shell. In the second case, a degradable macromonomer obtained by the ring opening polymerization of lactide using 2‐hydroxyethyl methacrylate as initiator is used as the core‐forming monomer to obtain degradable RDPPs. In both cases, the particles are synthesized with a two‐step emulsion polymerization process conducted in one pot and then spray‐dried to obtain the RDPPs of interest. The morphology and redispersibility of the powders are characterized. Finally, their use as concrete additives is preliminarily assessed by evaluating their effect on changes in the surface morphologies of concrete specimens. [ABSTRACT FROM AUTHOR]

In this article, we deal with optimal dynamic carbon emission regulation of a set of firms. On the one hand, the regulator dynamically allocates emission allowances to each firm. On the other hand, firms face idiosyncratic, as well as common, economic shocks on emissions, and they have linear quadratic abatement costs. Firms can trade allowances so as to minimize total expected costs, which arise from abatement, trading, and terminal penalty. Using variational methods, we first exhibit in closed form the market equilibrium in function of the regulator's dynamic allocation. We then solve the Stackelberg game between the regulator and the firms. The result is a closed‐form expression of the optimal dynamic allocation policies that allow a desired expected emission reduction. The optimal policy is unique in the presence of market impact. In absence of market impact, the optimal policy is nonunique, but all the optimal policies share common properties. The optimal policies are fully responsive, and therefore induce a constant abatement effort and a constant price of allowances. Our results are robust to some extensions, like different penalty functions. [ABSTRACT FROM AUTHOR]

This article examines neural network‐based approximations for the superhedging price process of a contingent claim in a discrete time market model. First we prove that the α‐quantile hedging price converges to the superhedging price at time 0 for α tending to 1, and show that the α‐quantile hedging price can be approximated by a neural network‐based price. This provides a neural network‐based approximation for the superhedging price at time 0 and also the superhedging strategy up to maturity. To obtain the superhedging price process for t>0$t>0$, by using the Doob decomposition, it is sufficient to determine the process of consumption. We show that it can be approximated by the essential supremum over a set of neural networks. Finally, we present numerical results. [ABSTRACT FROM AUTHOR]

Background: Several genetic models that recapitulate neurodegenerative features of Parkinson's disease (PD) exist, which have been largely based on genes discovered in monogenic PD families. However, spontaneous genetic mutations have not been linked to the pathological hallmarks of PD in non‐human vertebrates. Objective: To describe the genetic and pathological findings of three Yellow‐crowned parrot (Amazona ochrocepahala) siblings with a severe and rapidly progressive neurological phenotype. Methods: The phenotype of the three parrots included severe ataxia, rigidity, and tremor, while their parents were phenotypically normal. Tests to identify avian viral infections and brain imaging studies were all negative. Due to their severe impairment, they were all euthanized at age 3 months and their brains underwent neuropathological examination and proteasome activity assays. Whole genome sequencing (WGS) was performed on the three affected parrots and their parents. Results: The brains of affected parrots exhibited neuronal loss, spongiosis, and widespread Lewy body‐like inclusions in many regions including the midbrain, basal ganglia, and neocortex. Proteasome activity was significantly reduced in these animals compared to a control (P < 0.05). WGS identified a single homozygous missense mutation (p.V559L) in a highly conserved amino acid within the pleckstrin homology (PH) domain of the calcium‐dependent secretion activator 2 (CADPS2) gene. Conclusions: Our data suggest that a homozygous mutation in the CADPS2 gene causes a severe neurodegenerative phenotype with Lewy body‐like pathology in parrots. Although CADPS2 variants have not been reported to cause PD, further investigation of the gene might provide important insights into the pathophysiology of Lewy body disorders. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA. [ABSTRACT FROM AUTHOR]

Herein, we report on an individual with molecularly confirmed diagnosis of NS showing asymptomatic enlarged spinal nerve roots, which are distinctive features of neurofibromatosis type 1. 3 Ando Y, Sawada M, Kawakami T, Morita M, Aoki Y. A patient with Noonan syndrome with a KRAS mutation who presented severe nerve root hypertrophy. Noonan syndrome (NS) belongs to RASopathies, a family of disorders caused by unregulated signaling through the RAS-MAPK pathway. [Extracted from the article]

Aim: To investigate the prevalence of amyloid cardiomyopathy (AC) and the diagnostic accuracy of echocardiographic red flags of AC among consecutive adult patients undergoing transthoracic echocardiogram for reason other than AC in 13 Italian institutions. Methods and results: This is an Italian prospective multicentre study, involving a clinical and instrumental work‐up to assess AC prevalence among patients ≥55 years old with an echocardiogram suggestive of AC (i.e. at least one echocardiographic red flag of AC in hypertrophic, non‐dilated left ventricles with preserved ejection fraction). The study was registered at ClinicalTrials.gov (NCT04738266). Overall, 381 patients with an echocardiogram suggestive of AC were identified among a cohort of 5315 screened subjects, and 217 patients completed the investigations. A final diagnosis of AC was made in 62 patients with an estimated prevalence of 29% (95% confidence interval 23%–35%). Transthyretin‐related AC (ATTR‐AC) was diagnosed in 51 and light chain‐related AC (AL‐AC) in 11 patients. Either apical sparing or a combination of ≥2 other echocardiographic red flags, excluding interatrial septum thickness, provided a diagnostic accuracy >70%. Conclusion: In a cohort of consecutive adults with echocardiographic findings suggestive of AC and preserved left ventricular ejection fraction, the prevalence of AC (either ATTR or AL) was 29%. Easily available echocardiographic red flags, when combined together, demonstrated good diagnostic accuracy. [ABSTRACT FROM AUTHOR]

Keywords: asthma; epithelial cells; IL-17A; paediatrics EN asthma epithelial cells IL-17A paediatrics 569 573 5 04/04/22 20220401 NES 220401 To the Editor, Although asthma is often associated with cytokines typically produced by Th2 cells, the "T2 paradigm" is unable to explain the full spectrum of asthma severity; indeed, "severe" asthmatics often display inflammatory profiles consistent with mixed T2/T17 inflammation.1 Using a mouse model of asthma, we have shown that while severe asthma-like disease is associated with expansion of both Th2 and Th17 cells, increased production of Th17-associated cytokines are accompanied by increased measures of IL-17A-induced cellular activation (intracellular signalling, IL-17A-induced gene expression) in lung structural cells.2 These findings suggest that intrinsic differences in IL-17A responsiveness may contribute to the development of more severe asthma independently of changes in IL-17A production. The goals of the current study were to identify clinical factors associated with IL-17A responsiveness in children with asthma, and determine if IL-17A responsiveness differs in nasal epithelial cells from children with mild, moderate and severe asthma. To our knowledge, this represents the first attempt to determine if nasal epithelial cell responsiveness to IL-17A is associated with asthma-relevant clinical parameters, or asthma severity. However, our results demonstrate that increased IL-17A-induced CXCL1 production is comparable in children with different asthma severities, suggesting that increased epithelial cell responsiveness to IL-17A may be a general marker of asthma pathogenesis and not a marker of severe asthma as proposed by Andersson et al. [Extracted from the article]

The novel HLA‐DPA1*01:195 allele differs from HLA‐DPA1*01:03:01:01 by one nucleotide substitution in exon 4. [ABSTRACT FROM AUTHOR]

Introduction: The identification of dementia cases through routinely collected health data represents an easily accessible and inexpensive method to estimate the prevalence of dementia. In Italy, a project aimed at the validation of an algorithm was conducted. Methods: The project included cases (patients with dementia or mild cognitive impairment [MCI]) recruited in centers for cognitive disorders and dementias and controls recruited in outpatient units of geriatrics and neurology. The algorithm based on pharmaceutical prescriptions, hospital discharge records, residential long-term care records, and information on exemption from health-care co-payment, was applied to the validation population. Results: The main analysis was conducted on 1110 cases and 1114 controls. The sensitivity, specificity, and positive and negative predictive values in discerning cases of dementia were 74.5%, 96.0%, 94.9%, and 79.1%, respectively, whereas in detecting cases of MCI these values were 29.7%, 97.5%, 92.2%, and 58.1%, respectively. The variables associated with misclassification of cases were also identified. Discussion: This study provided a validated algorithm, based on administrative data, which can be used to identify caseswith dementia and, with lower sensitivity, also early onset dementia but not cases withMCI. [ABSTRACT FROM AUTHOR]

This paper assesses the risk of a mass lapse event in life insurance. The rarity of the event and the complexity of policyholder behavior make the risk assessment of such a scenario difficult. Using a simulation study, we evaluate how different estimation methods can assess the risk of this scenario, using panel data at the company level. We then use the best‐performing method to estimate the probability distribution function of a mass cancellation event in the United States and Germany. We identify dependencies of the event on company and country characteristics, which have not been taken into account by regulating agencies. We also find that the current mass lapse scenario in Solvency II has no empirical foundation for the German market. We show that an empirically valid scenario leads to a significantly lower solvency capital requirement for the average German life insurer. [ABSTRACT FROM AUTHOR]

The industrialization of perovskite solar cells relies on solving intrinsic‐to‐material issues. To reach record efficiencies perovskite deposition needs to be finely adjusted by multi‐step processes, in a humidity free glove‐box environment and by means of hardly scalable techniques often associated with toxic solvents and anti‐solvent dripping/bath. Herein, the use of polymeric material is proposed to deposit perovskite layers with easy processability. To the scope, a starch‐polymer/perovskite composite is developed to suit slot‐die coating technique requirement, allowing the deposition of hybrid halide perovskite material in a single straightforward step without the use of toxic solvents, and in uncontrolled humid environment (RH up to 70 %). The starch‐polymer increases the viscosity of the perovskite precursor solutions and delays the perovskite crystallization that results in the formation of perovskite films at mild temperature (60 °C) with good morphology. These innovative inks enables the fabrication of flexible solar cells with p‐i‐n configuration featured by a power conversion efficiency higher than 3 %.. Overall, this approach can be exploited in the future to massively reduce perovskite manufacturing costs related to keeping the entire fabrication line at high‐temperature and under nitrogen or dry conditions. [ABSTRACT FROM AUTHOR]

Aims: In patients with heart failure and reduced ejection fraction (HFrEF) and secondary mitral regurgitation (SMR), impaired right ventricular function (RVF) may negatively influence the prognosis. Percutaneous mitral valve repair (pMVR) can promote the recovery of RVF. We sought to characterize the response of the right ventricle to pMVR in HFrEF with SMR and to assess the association between improved RVF after pMVR and outcomes.Methods and Results: Overall, 221 patients with HFrEF and SMR ≥3+ successfully treated with pMVR in four tertiary care centres for heart failure were included. Improved RVF was defined as Δ right ventricular fractional area change (ΔRVFAC) ≥5% at early follow-up (median time 4 months). The primary endpoint was a composite of death/heart transplantation (D/HT). Mean age was 69 ± 11 years, mean left ventricular ejection fraction was 31 ± 8% and mean RVFAC was 34 ± 9%. ΔRVFAC ≥5% occurred in 88 patients (40%) and was independent of the measures of left ventricular reverse remodelling. During a median follow-up of 29 months (interquartile range 12-46), 81 patients (37%) reached the primary endpoint. After adjustment for other significant covariates, ΔRVFAC ≥5% was significantly associated with lower risk of D/HT (hazard ratio 0.52, 95% confidence interval 0.29-0.94, P = 0.030). In the secondary outcome analysis exploring the risk of heart failure hospitalizations, ΔRVFAC ≥5% confirmed the prognostic association with the endpoint.Conclusions: In patients with HFrEF and SMR, about 40% of patients improved RVF after pMVR. RVF improvement was associated with better long-term survival free from HT and lower risk of heart failure hospitalization. [ABSTRACT FROM AUTHOR]

The interactive effect of silicon (Si) application on soil fertility is poorly understood when inoculation with Azospirillum brasilense is performed. This research determined if Si application and A. brasilense inoculation to corn (Zea mays L.) and wheat (Triticum aestivum L.) has agronomic benefits on soil nutrient concentration and grain yield. Treatments were tested under a no-till system in a Rhodic Haplustox in a full factorial design with four replicates and comprised (a) two soil amendment sources--calcium (Ca) and magnesium (Mg) silicate and dolomitic limestone; (b) with and without seed inoculation with A. brasilense; and (c) five sampling dates collected during two corn-wheat crop rotations (2015-2017). Calcium and Mg silicate application was effective at decreasing soil hydrogen + aluminum (H+Al) and Al content and increasing soil pH, sum of bases, and base saturation. However, silicate changed soil nutrient availability, reduced cation exchange capacity, phosphorus (P) and Mg content and did not significantly affect (p > .05) corn and wheat grain yield. Inoculation reduced Al toxicity, with lower H+Al and Al contents, and increased K content, leading to a greater pH and base saturation after four cropping seasons. Inoculation increased corn and wheat grain yield by 8.2 and 8.3%, respectively. Application of Ca and Mg silicate was more effective than limestone as a liming agent but could result in decreased availability of certain nutrients in soil. Inoculation with A. brasilense could be an important management practice to maintain adequate Si content in soil when limestone is applied. However, with silicate application, A. brasilense could increase Si depletion in soil. [ABSTRACT FROM AUTHOR]

Background and purpose: In patients with acute ischemic stroke treated with reperfusion therapy we aimed to evaluate whether pretreatment blood–brain barrier (BBB) leakage is associated with subsequent hemorrhagic transformation (HT). Methods: We prospectively screened patients with acute ischemic stroke treated with intravenous thrombolysis and/or endovascular treatment. Before treatment, each patient received computed tomography (CT), CT angiography, and CT perfusion. We assessed pretreatment BBB leakage within the ischemic area using the volume transfer constant (Ktrans) value. Our primary outcome was relevant HT, defined as hemorrhagic infarction type 2 or parenchymal hemorrhage type 1 or 2. We evaluated independent associations between BBB leakage and HT using logistic regression, adjusting for age, sex, baseline stroke severity, Alberta Stroke Program Early CT Score (ASPECTS) ≥ 6, treatment type, and onset‐to‐treatment time. Results: We enrolled 171 patients with available assessment of BBB leakage. The patients' mean (±SD) age was 75.5 (±11.8) years, 86 (50%) were men, and the median (interquartile range) National Institutes of Health Stroke Scale score was 18 (12–23). A total of 32 patients (18%) received intravenous thrombolysis, 102 (60%) underwent direct endovascular treatment, and 37 (22%) underwent both. Patients with relevant HT (N = 31;18%) had greater mean BBB leakage (Ktrans 0.77 vs. 0.60; p = 0.027). After adjustment in the logistic regression model, we found that BBB leakage was associated both with a more than twofold risk of relevant HT (odds ratio [OR] 2.50; 95% confidence interval [CI] 1.03–6.03 per Ktrans point increase; OR 2.34; 95% CI 1.06–5.17 for Ktrans values > 0.63 [mean BBB leakage value]) and with symptomatic intracerebral hemorrhage (OR 4.30; 95% CI 1.13–13.77 per Ktrans point increase). Conclusion: Pretreatment BBB leakage before reperfusion therapy was associated with HT, and may help to identify patients at risk of HT. [ABSTRACT FROM AUTHOR]

Aims: The use of beta‐blocker therapy in cardiac amyloidosis (CA) is debated. We aimed at describing patterns of beta‐blocker prescription through a nationwide survey. Methods and results: From 11 referral centres, we retrospectively collected data of CA patients with a first evaluation after 2016 (n = 642). Clinical characteristics at first and last evaluation were collected, with a focus on medical therapy. For patients in whom beta‐blocker therapy was started, stopped, or continued between first and last evaluation, the main reason for beta‐blocker management was requested. Median age of study population was 77 years; 81% were men. Arterial hypertension was found in 58% of patients, atrial fibrillation (AF) in 57%, and coronary artery disease in 16%. Left ventricular ejection fraction was preserved in 62% of cases, and 74% of patients had advanced diastolic dysfunction. Out of the 250 CA patients on beta‐blockers at last evaluation, 215 (33%) were already taking this therapy at first evaluation, while 35 (5%) were started it, in both cases primarily because of high‐rate AF. One‐hundred‐nineteen patients (19%) who were on beta‐blocker at first evaluation had this therapy withdrawn, mainly because of intolerance in the presence of heart failure with advanced diastolic dysfunction. The remaining 273 patients (43%) had never received beta‐blocker therapy. Beta‐blockers usage was similar between CA aetiologies. Patients taking vs. not taking beta‐blockers differed only for a greater prevalence of arterial hypertension, coronary artery disease, AF, and non‐restrictive filling pattern (P < 0.01 for all) in the former group. Conclusions: Beta‐blockers prescription is not infrequent in CA. Such therapy may be tolerated in the presence of co‐morbidities for which beta‐blockers are routinely used and in the absence of advanced diastolic dysfunction. [ABSTRACT FROM AUTHOR]

Severe eosinophilic asthma (SEA) has been associated with T‐helper type 2 (Th2) inflammatory response. A good understanding of T cell functions in asthma is important for therapy, especially in the choice of biological treatments for severe cases. Mepolizumab, an IL‐5 antagonist, is indicated for the treatment of severe asthma. Regulatory T cells (Tregs) suppress inflammation by secreting cytokines that inhibit Th2 cell proliferation. We investigated peripheral Treg, CD4, CD8, CD19 and NK cell percentages and their relationship to clinical and functional parameters, including peripheral eosinophils, before and after anti‐IL5 treatment. Subjects were 14 adult SEA patients (9 male, 54.1 ± 11.6 years), treated with mepolizumab, and 10 controls. T cells (CD4 and CD8), CD19, NK and Tregs were evaluated by flow cytometry. Comparison of lung function parameters before and after treatment with mepolizumab (T0 and T1) showed an increase in FEV1, FEV1/FVC ratio and a reduction in blood eosinophil percentages. CD8 and CD16/56+CD3+ were significantly higher in SEA patients than controls (P =.04 and P =.03, respectively). A decrease in CD45+, CD8 + and CD16/56+CD3+ cell percentages was observed between T0 and T1 (P =.02, P =.04, P =.03, respectively). A significant increase in Treg percentages (P =.0001) was recorded between T0 and T1. Mepolizumab therapy was found to modulate immune response, restoring immune balance in patients with SEA. [ABSTRACT FROM AUTHOR]

Background: Second‐hand smoke (SHS) exposure is associated with paediatric asthma, and oxidative stress is believed to play a role in mediating this association. The nuclear factor (erythroid‐derived 2)‐like 2 (NFE2L2) is important for the defence against oxidative stress. Objective: To explore interactions between NFE2L2 genotype and SHS exposure in paediatric asthma risk. Methods: We used a genotyped subset of patients of European ancestry (N = 669, median age at enrolment = 6.8 years) enrolled in the clinical cohort Greater Cincinnati Pediatric Clinic Repository as the study population, and a population‐based paediatric cohort (N = 791) to replicate our findings. History of asthma diagnosis was obtained from medical records, and SHS exposure was obtained from questionnaires. Four NFE2L2 tagging SNPs were included in the analysis, and interactions between SHS and NFE2L2 genotype were evaluated using logistic regression. Results: Three of the analysed SNPs, rs10183914, rs1806649 and rs2886161, interacted significantly with SHS exposure to increase asthma risk (p ≤.02). The interaction was replicated in an independent cohort for rs10183914 (p =.04). Interactions between SHS exposure and NFE2L2 genotype were also associated with an increased risk of hospitalization (p =.016). In stratified analyses, NFE2L2 genotype was associated with daily asthma symptoms in children with SHS exposure (OR = 3.1; p =.048). No association was found in children without SHS exposure. Examination of publicly available chromatin immunoprecipitation followed by sequencing (ChIP‐seq) data sets confirmed the presence of active histone marks and binding sites for particular transcription factors overlapping the coordinates for the significantly associated SNPs. Conclusions and Clinical Relevance: Our study provides evidence that NFE2L2 genotype interacts with SHS exposure to affect both asthma risk and severity in children and identifies a population of children at increased risk of asthma development. [ABSTRACT FROM AUTHOR]

Background: Asthma is highly heterogeneous, and severity evaluation is key to asthma management. DNA methylation (DNAm) contributes to asthma pathogenesis. This study aimed to identify nasal epithelial DNAm differences between severe and nonsevere asthmatic children and evaluate the impact of environmental exposures. Methods: Thirty‐three nonsevere and 22 severe asthmatic African American children were included in an epigenome‐wide association study. Genome‐wide nasal epithelial DNAm and gene expression were measured. CpG sites associated with asthma severity and environmental exposures and predictive of severe asthma were identified. DNAm was correlated with gene expression. Enrichment for transcription factor (TF) binding sites or histone modifications surrounding DNAm differences were determined. Results: We identified 816 differentially methylated CpG positions (DMPs) and 10 differentially methylated regions (DMRs) associated with asthma severity. Three DMPs exhibited discriminatory ability for severe asthma. Intriguingly, six DMPs were simultaneously associated with asthma, allergic asthma, total IgE, environmental IgE, and FeNO in an independent cohort of children. Twenty‐seven DMPs were associated with traffic‐related air pollution or secondhand smoke. DNAm at 22 DMPs was altered by diesel particles or allergen in human bronchial epithelial cells. DNAm levels at 39 DMPs were correlated with mRNA expression. Proximal to 816 DMPs, three histone marks and several TFs involved in asthma pathogenesis were enriched. Conclusions: Significant differences in nasal epithelial DNAm were observed between nonsevere and severe asthma in African American children, a subset of which may be useful to predict disease severity. These CpG sites are subjected to the influences of environmental exposures and may regulate gene expression. [ABSTRACT FROM AUTHOR]

Background: Children with atopic dermatitis (AD) are often sensitized to food and aeroallergens, but sensitization patterns have not been analysed with biologic measures of disease pathogenicity. Objective: We sought to define allergen sensitization grouping(s) using unbiased machine learning and determine their associations with skin filaggrin (FLG) and transepidermal water loss (TEWL) (assesses skin barrier integrity), S100A8 and S100A9 expression (assesses skin inflammation) and AD severity. Methods: We studied 400 children with AD in the Mechanisms of Progression from Atopic Dermatitis to Asthma in Children (MPAACH) cohort to identify groupings of food and aeroallergen sensitizations. MPAACH is a paediatric AD cohort, aged 1–2, recruited through hospital/community settings between 2016 and 2018. We analysed these groupings' associations with AD biomarkers: skin FLG, S100A8 and S100A9 expression, total IgE, TEWL and AD severity. Results: An unbiased machine learning approach revealed five allergen clusters. The most common cluster (N = 131), SPTPEP, had sensitization to peanut, egg and/or pets. Three low prevalence clusters, which included children with allergen sensitization other than peanut, egg or pets, were combined into SPTOther. SPTNEG included children with no sensitization(s). SPTPEP children had higher median non‐lesional TEWL (16.9 g/m2/h) and IgE (90 kU/L) compared with SPTOTHER (8.8 g/m2/h and 24 kU/L; p =.01 and p <.001) and SPTNEG (9 g/m2/h and 26 kU/L; p =.003 and p <.001). SPTPEP children had lower median lesional (0.70) and non‐lesional (1.09) FLG expression compared with SPTOTHER (lesional: 0.9; p =.047, non‐lesional: 1.78; p =.01) and SPTNEG (lesional: 1.47; p <.001, non‐lesional: 2.21; p <.001). There were no differences among groupings in S100A8 or S100A9 expression. Conclusions and clinical relevance: In this largely clinic‐based cohort of young children with AD, allergic sensitization to peanut, egg, cat or dog was associated with more severe disease and skin barrier function but not markers of cutaneous inflammation. These data need replicating in a population‐based cohort but may have important implications for understanding the interaction between AD and allergic sensitization. [ABSTRACT FROM AUTHOR]

Background: Atopic dermatitis (AD) patients are often colonized with Staphylococcus aureus, and staphylococcal biofilms have been reported on adult AD skin lesions. The commensal S epidermidis can antagonize S aureus, although its role in AD is unclear. We sought to characterize S aureus and S epidermidis colonization and biofilm propensity and determine their associations with AD severity, barrier function, and epidermal gene expression in the first US early‐life cohort of children with AD, the Mechanisms of Progression of Atopic Dermatitis to Asthma in Children (MPAACH). Methods: The biofilm propensity of staphylococcal isolates was assessed by crystal violet assays. Gene expression of filaggrin and antimicrobial alarmins S100A8 and S100A9 was measured in keratinocyte RNA extracted from skin tape strips. Staphylococcal biofilms sampled from MPAACH skin were visualized using scanning electron microscopy. Results: Sixty‐two percent of staphylococcal isolates (sampled from 400 subjects) formed moderate/strong biofilms. Sixty‐eight percent of subjects co‐colonized with both staphylococcal species exhibited strains that formed cooperative mixed‐species biofilms. Scanning electron microscopy verified the presence of staphylococcal biofilms on the skin of MPAACH children. Staphylococcus aureus strains showing higher relative biofilm propensity compared with S epidermidis were associated with increased AD severity (P =.03) and increased lesional and nonlesional transepidermal water loss (P =.01, P =.03). Conclusions: Our data suggest a pathogenic role for S aureus biofilms in AD. We found that strain‐level variation in staphylococcal isolates governs the interactions between S epidermidis and S aureus and that the balance between these two species, and their biofilm propensity, has important implications for AD. [ABSTRACT FROM AUTHOR]

The cytochrome bc1 complex is a key component of the mitochondrial respiratory chains of many eukaryotic microorganisms that are pathogenic for plants or humans, such as fungi responsible for crop diseases and Plasmodium falciparum, which causes human malaria. Cytochrome bc1 is an enzyme that contains two (ubi)quinone/quinol‐binding sites, which can be exploited for the development of fungicidal and chemotherapeutic agents. Here, we review recent progress in determination of the structure and mechanism of action of cytochrome bc1, and the associated development of antimicrobial agents (and associated resistance mechanisms) targeting its activity. [ABSTRACT FROM AUTHOR]

As a multi‐objective policy, the EU Common Agricultural Policy continues to secure significant income support for farmers as one of the nine specific objectives. We estimate the income transfer efficiency of a broad set of pivotal policy measures, focusing on the effects of farm structure on income transfer efficiency. We use dynamic modelling, based on a micro‐data panel of Italian farms for the period 2008–2014, allowing for endogeneity, simultaneity bias, and omitted variables. In line with previous studies and economic expectations, we find that decoupled direct payments provide the highest contribution to agricultural incomes, followed by agri‐environmental payments and on‐farm investment subsidies. Coupled payments have no significant impacts on farmers' income. Generally, for all analysed Common Agricultural Policy measures, large farms benefit from greater transfer efficiency levels compared with medium and small farms. These differences among instruments and across farms suggest that policy‐participation costs may play a pivotal role, together with the economic structure of farms, in determining the income transfer efficiency of CAP policies. [ABSTRACT FROM AUTHOR]

Neurosteroids can modulate γ‐aminobutyric acid type A receptor‐mediated inhibitory currents. Recently, we discovered that the neurosteroids progesterone, 5α‐dihydroprogesterone, allopregnanolone, and pregnanolone are reduced in the cerebrospinal fluid of patients with status epilepticus (SE). However, it is undetermined whether neurosteroids influence SE. For this reason, first we evaluated whether the inhibitor of adrenocortical steroid production trilostane (50 mg/kg) could modify the levels of neurosteroids in the hippocampus and neocortex, and we found a remarkable increase in pregnenolone, progesterone, 5α‐dihydroprogesterone, and allopregnanolone levels using liquid chromatography tandem mass spectrometry. Second, we characterized the dynamics of SE in the presence of the varied neurosteroidal milieu by a single intraperitoneal kainic acid (KA; 15 mg/kg) injection in trilostane‐treated rats and their controls. Convulsions started in advance in the trilostane group, already appearing 90 minutes after the KA injection. In contrast to controls, convulsions prevalently developed as generalized seizures with loss of posture in the trilostane group. However, this effect was transient, and convulsions waned 2 hours before the control group. Moreover, electrocorticographic traces of convulsions were shorter in trilostane‐treated rats, especially at the 180‐minute (P <.001) and 210‐minute (P <.01) time points. These findings indicate that endogenous neurosteroids remarkably modulate SE dynamics. [ABSTRACT FROM AUTHOR]

Aims: The optimization of guideline‐directed medical therapy (GDMT) in reduced ejection fraction heart failure (HFrEF) is associated with improved survival and can reduce the severity of secondary mitral regurgitation (SMR). Highest tolerated doses should be achieved before percutaneous mitral valve repair (pMVR) and drugs titration further pursued after procedure. The degree of GDMT titration in patients with HFrEF and SMR treated with pMVR remains unexplored. We sought to evaluate the adherence to GDMT in HFrEF in patients undergoing pMVR and to explore the association between changes in GDMT post‐pMVR and prognosis. Methods and results: We included all the patients with HFrEF and SMR ≥ 3 + treated with pMVR between 2012 and 2019 and with available follow‐up. GDMT, comprehensive of dosages, was systematically recorded. The study endpoint was a composite of death and heart transplantation. Among 133 patients successfully treated, 121 were included (67 ± 12 years old, 77% male patients). Treatment rates of angiotensin‐converting enzyme inhibitors/angiotensin receptor blockers/angiotensin receptor neprilysin inhibitor (ACEIs/ARBs/ARNI), beta‐blockers, and mineralcorticoid receptor antagonist at baseline and follow‐up were 73% and 79%, 85% and 84%, 70% and 70%, respectively. At baseline, 33% and 32% of patients were using >50% of the target dose of ACEI/ARB/ARNI and beta‐blockers. At follow‐up (median time 4 months), 33% of patients unchanged, 34% uptitrated, and 33% of patients downtitrated GDMT. Downtitration of GDMT was independently associated with higher risk of death/heart transplantation (hazard ratio: 2.542, 95%confidence interval: 1.377–4.694, P = 0.003). Conclusions: Guideline‐directed medical therapy is frequently underdosed in HFrEF patients with SMR undergoing pMVR. Downtitration of medications after procedure is associated with poor prognosis. [ABSTRACT FROM AUTHOR]

Natural molecular machines require a continuous fuel supply to perform motions and/or remain in a functional state. Consequently, the aim of developing artificial devices and materials with life‐type properties has motivated a growing interest in abiotic chemical fuels and in their supply modalities. Many artificial molecular machines have been developed in which the sequential addition of several chemical reagents allows the machine to perform complete cycles of motion. Only recently, examples of molecular machines whose cycles of motion are triggered by a single pulse of fuel have been reported. The latter systems are the object of this Minireview where the abiotic chemical fuels used so far to trigger the complete cycles of motion of molecular machines are described, with particular emphasis on the operation mechanism of the machine/fuel systems. [ABSTRACT FROM AUTHOR]

Objective. Atypical parathyroid adenoma is a rare neoplasm, showing atypical histological features intermediate between classic benign adenoma and the rarest parathyroid carcinoma, whose the clinical behaviour and outcome is not yet understood or predictable. Up to date only two cases of atypical adenoma were found associated to a MEN1 syndrome, and only one was proved to carry a pathogenic variant of the MEN1 gene. Design. We report the clinical, histologic, and molecular findings of a 44-year-old woman, presenting with a histologically proved atypical parathyroid adenoma with an apparent aggressive behaviour. Methods and Results. CDC73 gene was screened at germline and somatic levels with no results. Whole exome sequencing performed on DNA extracted from blood leukocytes and tumour tissue revealed a somatic MEN1 gene heterozygous variant, c.912+1G > A, of the splicing donor site of exon 6. On immunohistochemistry, downregulation of the menin protein expression in the neoplastic cells was also observed. Conclusions. We report the second case of a rare association of a somatic MEN1 gene mutation in a patient with atypical parathyroid adenoma. We suggest that MEN1 gene could be an underestimate genetic determinant of these rare histological entities, and we highlight the utility of a complete genetic screening protocol, by the use of next-generation sequencing technology in such undetermined clinical cases with no frank clinical presentation. [ABSTRACT FROM AUTHOR]

The novel HLA class II allele HLA‐DPB1*1485:01 is described. [ABSTRACT FROM AUTHOR]

Background: Achalasia is a rare idiopathic disease with a complex etio‐pathogenesis still unknown. This study aimed to identify microRNA (miRNA)‐mRNA regulatory networks underlying achalasia. Methods: The investigation was performed in tissue specimens from 11 patients and five controls using the microarray technology followed by an integrated bioinformatics analysis. Key Results: One hundred and six miRNAs were significantly up‐regulated and 64 were down‐regulated in achalasia patients. The expression of the most 10 differential expressed miRNAs (miR‐122‐5p, miR‐133a‐3p, miR‐504‐5p, miR‐187‐3p, miR‐133b, miR‐200c‐3p, miR‐375, miR‐200b‐5p, miR‐200b‐3p, and miR203a) was confirmed by droplet digital PCR in an independent cohort. The interactions between the significant miRNAs and their targets uncovered 14 miRNA‐mRNA interacting pairs with experimentally predicted genes (ie, FN1, ROCK2, DPYSL2), and 35 pairs with not experimentally target genes (ie, SULF1, MRVI1, PRKG1); all genes were involved in immune cell trafficking, skeletal and muscular system development, nervous system development macro‐processes. Conclusion & Inferences: The mRNA–miRNA regulatory networks described in this study provide new insights in the genetic background of the disease, suggesting further investigations in novel pathogenic mechanisms. [ABSTRACT FROM AUTHOR]

In this paper, we report further progress toward a complete theory of state‐independent expected utility maximization with semimartingale price processes for arbitrary utility function. Without any technical assumptions, we establish a surprising Fenchel duality result on conjugate Orlicz spaces, offering a new economic insight into the nature of primal optima and providing a fresh perspective on the classical papers of Kramkov and Schachermayer. The analysis points to an intriguing interplay between no‐arbitrage conditions and standard convex optimization and motivates the study of the fundamental theorem of asset pricing for Orlicz tame strategies. [ABSTRACT FROM AUTHOR]

This work aimed to render phenomenologically autonomous the otherwise stepwise operation of a catenane‐based molecular switch, which is chemically triggered by the decarboxylation of 2‐cyano‐2‐phenylpropanoic acid (2). Given that any amount of 2 in stoichiometric excess with respect to the catenane is consumed in a side reaction, the authors resorted to the corresponding anhydride 5, the slow hydrolysis of which, due to adventitious water in dichloromethane, continuously produces in situ the actual fuel 2. As a consequence, the machine does not require a reloading after each cycle, but switches back and forth as long as fuel is present. [ABSTRACT FROM AUTHOR]

This study focuses on the appropriate design of the inductive elements of the LLC converter based on a typical industrial approach, i.e. assuming to use standard parts available on the market from qualified manufacturers. At first, a methodology to select the passive components is presented, highlighting the difference between the external inductor solution and the magnetically integrated solution. Secondly the step-by-step procedure used for the design of the high frequency transformer is illustrated. The possibility to integrate the resonant inductors into the HF transformer is then analysed, presenting different solutions. Finally a comparison between a classical and an integrated design is then presented referring to a case study; thus permitting to endow the potential benefits of the integrated solution. [ABSTRACT FROM AUTHOR]

We report on catalysis by a fuel‐induced transient state of a synthetic molecular machine. A [2]rotaxane molecular shuttle containing secondary ammonium/amine and thiourea stations is converted between catalytically inactive and active states by pulses of a chemical fuel (trichloroacetic acid), which is itself decomposed by the machine and/or the presence of additional base. The ON‐state of the rotaxane catalyzes the reduction of a nitrostyrene by transfer hydrogenation. By varying the amount of fuel added, the lifetime of the rotaxane ON‐state can be regulated and temporal control of catalysis achieved. The system can be pulsed with chemical fuel several times in succession, with each pulse activating catalysis for a time period determined by the amount of fuel added. Dissipative catalysis by synthetic molecular machines has implications for the future design of networks that feature communication and signaling between the components. [ABSTRACT FROM AUTHOR]

Background: The "atopic march" has been considered a linear progression starting with eczema and culminating with development of asthma. Not all asthma cases, however, are preceded by eczema, and not all children with eczema go on to develop asthma. Objective: The aim of this study was to explore the impact of allergic sensitization patterns on the association between early eczema and later childhood asthma. Given the numerous reported associations of the ciliary gene KIF3A with the atopic march, we also examined the impact of KIF3A risk allele rs12186803 on our analyses. Methods: We studied 505 participants in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS), a prospective birth cohort, with longitudinal eczema and asthma outcomes as well as prospective data regarding timing of sensitization to foods and aeroallergens. KIF3A genotypes were available on all children. Results: Two high‐risk groups were identified: one with and one without early eczema. The high‐risk group with early eczema was more likely to be sensitized to food allergens, while the group without early eczema was more likely to be polysensitized to aeroallergens. The KIF3A rs12186803 risk allele interacted with food sensitization to increase asthma risk in children with eczema (P = 0.02). In children without eczema, asthma was associated with the interaction between rs12186803 and aeroallergen sensitization (P = 0.007). Conclusions & Clinical Relevance: KIF3A interacted differentially with sensitization pattern to increase the risk of asthma in two high‐risk groups of children with and without early eczema. Given the reported role of KIF3A in epithelial cell functioning, the results add evidence to the hypothesis that an impaired epithelial barrier is a key aspect in the development of allergic disease. [ABSTRACT FROM AUTHOR]