Influence of Different Stabilization Systems and Multiple Ultraviolet A (UVA) Aging/Recycling Steps on Physicochemical, Mechanical, Colorimetric, and Thermal-Oxidative Properties of ABS

Commercially mass-polymerized acrylonitrile–butadiene–styrene (ABS) polymers, pristine or modified by stabilization systems, have been injection molded and repeatedly exposed to ultraviolet A (UVA) radiation, mechanical recycling, and extra injection molding steps to study the impact of such treatments on the physicochemical, mechanical, colorimetric, and thermal-oxidative characteristics. The work focus on mimicking the effect of solar radiation behind a window glass as relevant during the lifetime of ABS polymers incorporated in electrical and electronic equipment, and interior automotive parts by using UVA technique. The accelerated aging promotes degradation and embrittlement of the surface exposed to radiation and causes physical aging, deteriorating mechanical properties, with an expressive reduction of impact strength (unnotched: up to 900%; notched: up to 250%) and strain at break (>1000%), as well as an increase in the yellowing index (e.g., 600%). UV-exposition promotes a slight increase in the tensile modulus (e.g., 10%). The addition of antioxidants (AOs) leads to a limited stabilization during the first UVA aging, although the proper AO formulation increases the thermal-oxidative resistance during all the cycles. Mechanical recycling promotes an increase in strain at break and unnotched impact strength alongside a slight decrease in tensile modulus, due to disruption of the brittle surface and elimination of the physical aging.This research was funded by the European Union’s Horizon 2020 Research and Innovation Program, grant number 730308

Pushing forward the predictive power of kinetic Monte Carlo simulations for detailed (de)polymerization chemistries

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Performance analysis of kinetic Monte Carlo algorithms for synthesis of linear polymers

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A20/TNFAIP3 heterozygosity predisposes to behavioral symptoms in a mouse model for neuropsychiatric lupus

Background: Neuropsychiatric lupus (NPSLE) refers to the neurological and psychiatric manifestations that are commonly observed in patients with systemic lupus erythematosus (SLE). An important question regarding the pathogenesis of NPSLE is whether the symptoms are caused primarily by CNS-intrinsic mechanisms or develop as a consequence of systemic autoimmunity. Currently used spontaneous mouse models for SLE have already contributed significantly to unraveling how systemic immunity affects the CNS. However, they are less suited when interested in CNS primary mechanisms. In addition, none of these models are based on genes that are associated with SLE. In this study, we evaluate the influence of A20, a well-known susceptibility locus for SLE, on behavior and CNS-associated changes in inflammatory markers. Furthermore, given the importance of environmental triggers for disease onset and progression, the influence of an acute immunological challenge was evaluated. Methods: Female and male A20 heterozygous mice (A20+/−) and wildtype littermates were tested in an extensive behavioral battery. This was done at the age of 10±2weeks and 24 ​± ​2 weeks to evaluate the impact of aging. To investigate the contribution of an acute immunological challenge, LPS was injected intracerebroventricularly at the age of 10±2weeks followed by behavioral analysis. Underlying molecular mechanisms were evaluated in gene expression assays on hippocampus and cortex. White blood cell count and blood-brain barrier permeability were analyzed to determine whether peripheral inflammation is a relevant factor. Results: A20 heterozygosity predisposes to cognitive symptoms that were observed at the age of 10 ​± ​2 weeks and 24 ​± ​2 weeks. Young A20+/− males and females showed a subtle cognitive phenotype (10±2weeks) with distinct neuroinflammatory phenotypes. Aging was associated with clear neuroinflammation in female A20+/− mice only. The genetic predisposition in combination with an environmental stimulus exacerbates the behavioral impairments related to anxiety, cognitive dysfunction and sensorimotor gating. This was predominantly observed in females. Furthermore, signs of neuroinflammation were solely observed in female A20+/− mice. All above observations were made in the absence of peripheral inflammation and of changes in blood-brain barrier permeability, thus consistent with the CNS-primary hypothesis. Conclusions: We show that A20 heterozygosity is a predisposing factor for NPSLE. Further mechanistic insight and possible therapeutic interventions can be studied in this mouse model that recapitulates several key hallmarks of the disease

Feature- versus rule-based generalization in rats, pigeons and humans

Humans can spontaneously create rules that allow them to efficiently generalize what they have learned to novel situations. An enduring question is whether rule-based generalization is uniquely human or whether other animals can also abstract rules and apply them to novel situations. In recent years, there have been a number of high-profile claims that animals such as rats can learn rules. Most of those claims are quite weak because it is possible to demonstrate that simple associative systems (which do not learn rules) can account for the behavior in those tasks. Using a procedure that allows us to clearly distinguish feature-based from rule-based generalization (the Shanks-Darby procedure), we demonstrate that adult humans show rule-based generalization in this task, while generalization in rats and pigeons was based on featural overlap between stimuli. In brief, when learning that a stimulus made of two components ("AB") predicts a different outcome than its elements ("A" and "B"), people spontaneously abstract an opposites rule and apply it to new stimuli (e.g., knowing that "C" and "D" predict one outcome, they will predict that "CD" predicts the opposite outcome). Rats and pigeons show the reverse behavior-they generalize what they have learned, but on the basis of similarity (e.g., "CD" is similar to "C" and "D", so the same outcome is predicted for the compound stimulus as for the components). Genuinely rule-based behavior is observed in humans, but not in rats and pigeons, in the current procedure

How increasingly powerful PRE modeling tools allow to unlock the full potential of FRP and RDRP in aqueous emulsion

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A novel interpretation of measured and simulated PLP data

Figure 1 - Simulated ν dependency of the observed kp in vinyl acetate PLP at 323 K. Case 1 (♦): chain length independent head-to-tail prop., Case 2 (■): chain length dependent head-to-tail prop., Case 3 (●): chain length dependent head-to-tail, head-to-head, tail-to-tail, and tail-to-head prop., and Case 4 (▲): Case 3 with backbiting by head and tail radicals, and mid-chain prop. Pulsed laser polymerization (PLP) is an interesting technique to study individual reactions.1-4 In PLP, photoinitiator radical fragments are generated at laser pulses with a frequency ν (or dark time Δt = ν-1). Depending on the PLP conditions and the monomer type, the molar mass distribution (MMD) can possess specific characteristics, allowing the determination of intrinsic rate coefficients. Most known is that under well-chosen conditions a multimodal MMD with inflection points Lj (j = 1, 2, …) is obtained, allowing the determination of the propagation rate coefficient kp ([M]0: initial monomer concentration): (1) In this contribution, kinetic Monte Carlo (kMC) modeling is applied to allow a further understanding and exploitation of PLP. For PLP of acrylates, regression analysis to low frequency inflection point data at various solvent volume fractions is proposed as an additional new method to estimate the backbiting rate coefficient kbb.5 Moreover, it is demonstrated that photodissociation, chain initiation and termination reactivities can be extracted from the complete PLP MMD.6 For the first time, the ratio of MMD peak heights has been used for the fast and reliable estimation of the photodissociation quantum yield,Φ.7 For PLP of vinyl acetate a unique combination of ab initio calculated rate coefficients and kMC simulations is considered to explain the experimental8 ν dependency of the observed kp (cf. Case 4 in Figure 1; Eq. (1) with kpobs). Via a stepwise extension of the kMC model (cf. 4 cases in Figure 1), the ν dependency is attributed to backbiting of tail radicals formed via head-to-head propagation.9 In contrast to acrylates, backbiting of head radicals is shown to be kinetically insignificant in VAc PLP, further highlighting the chemical difference between both vinyl monomer types. Please click Additional Files below to see the full abstract

Deep neural network-based clustering of deformation curves reveals novel disease features in PLN pathogenic variant carriers

Echocardiographic deformation curves provide detailed information on myocardial function. Deep neural networks (DNNs) may enable automated detection of disease features in deformation curves, and improve the clinical assessment of these curves. We aimed to investigate whether an explainable DNN-based pipeline can be used to detect and visualize disease features in echocardiographic deformation curves of phospholamban (PLN) p.Arg14del variant carriers. A DNN was trained to discriminate PLN variant carriers (n = 278) from control subjects (n = 621) using raw deformation curves obtained by 2D-speckle tracking in the longitudinal axis. A visualization technique was used to identify the parts of these curves that were used by the DNN for classification. The PLN variant carriers were clustered according to the output of the visualization technique. The DNN showed excellent discriminatory performance (C-statistic 0.93 [95% CI 0.87–0.97]). We identified four clusters with PLN-associated disease features in the deformation curves. Two clusters showed previously described features: apical post-systolic shortening and reduced systolic strain. The two other clusters revealed novel features, both reflecting delayed relaxation. Additionally, a fifth cluster was identified containing variant carriers without disease features in the deformation curves, who were classified as controls by the DNN. This latter cluster had a very benign disease course regarding development of ventricular arrhythmias. Applying an explainable DNN-based pipeline to myocardial deformation curves enables automated detection and visualization of disease features. In PLN variant carriers, we discovered novel disease features which may improve individual risk stratification. Applying this approach to other diseases will further expand our knowledge on disease-specific deformation patterns. Graphical abstract: [Figure not available: see fulltext.] Overview of the deep neural network-based pipeline for feature detection in myocardial deformation curves. Firstly, phospholamban (PLN) p.Arg14del variant carriers and controls were selected and a deep neural network (DNN) was trained to detect the PLN variant carriers. Subsequently, a clustering-based approach was performed on the attention maps of the DNN, which revealed 4 distinct phenotypes of PLN variant carriers with different prognoses. Moreover, a cluster without features and a benign prognosis was detected

IFNβ Protects Neurons from Damage in a Murine Model of HIV-1 Associated Brain Injury.

Infection with human immunodeficiency virus-1 (HIV-1) causes brain injury. Type I interferons (IFNα/β) are critical mediators of any anti-viral immune response and IFNβ has been implicated in the temporary control of lentiviral infection in the brain. Here we show that transgenic mice expressing HIV-1 envelope glycoprotein 120 in their central nervous system (HIVgp120tg) mount a transient IFNβ response and provide evidence that IFNβ confers neuronal protection against HIVgp120 toxicity. In cerebrocortical cell cultures, neuroprotection by IFNβ against gp120 toxicity is dependent on IFNα receptor 1 (IFNAR1) and the β-chemokine CCL4, as IFNAR1 deficiency and neutralizing antibodies against CCL4, respectively, abolish the neuroprotective effects. We find in vivo that IFNβ mRNA is significantly increased in HIVgp120tg brains at 1.5, but not 3 or 6 months of age. However, a four-week intranasal IFNβ treatment of HIVgp120tg mice starting at 3.5 months of age increases expression of CCL4 and concomitantly protects neuronal dendrites and pre-synaptic terminals in cortex and hippocampus from gp120-induced damage. Moreover, in vivo and in vitro data suggests astrocytes are a major source of IFNβ-induced CCL4. Altogether, our results suggest exogenous IFNβ as a neuroprotective factor that has potential to ameliorate in vivo HIVgp120-induced brain injury