פרסומים

Herein, we report complementary computational and experimental evidence supporting the existence, for indan-1-ylidene malononitrile and fluoren-9-ylidene malononitrile, of a non-radiative decay channel involving double bond isomerisation motion. The results of UV-Vis transient absorption spectroscopy highlight that the decay takes place within hundreds of picoseconds. In order to understand the related molecular mechanism, photochemical reaction paths were computed by employing multiconfigurational quantum chemistry. The results indicate that the excited state deactivation occurs via concerted double bond twisting of the dicyanovinyl (DCV) unit coupled with a pyramidalisation of its substituted carbon. It is also shown that the observed differences in the excited state lifetimes when passing from indan-1-ylidene malononitrile to fluoren-9-ylidene are associated with the change in the topography of the conical intersection driving the decay from intermediate to sloped, respectively.

Despite its total reliance on its host plant, the holoparasitePhelipanche aegyptiacasuffers from a deficiency of aromatic amino acids upon exposure to glyphosate.

Although relating to the same system, the interpretations of the water spectra from Raman and Dielectric spectroscopy present independent pictures of the nature of water. We show that in the overlap region of the two methods it is possible to combine these views into a coherent concept of what drives the dynamic features of water. In this work, we develop the idea that the dielectric relaxation in water is driven by the migration of defects through the H-bond network, leading to a Debye-like peak in the lower frequencies. The deviation from the Debye law in the higher sub-THz frequencies is traced to a global fluctuation of the same H-bond network, clearly evident in the Raman Spectra. By incorporating these two views, a mathematical formalism is presented that can aptly explicate the dielectric spectra of liquid water.

When travelers book hotels online, they are typically provided with a list of relevant hotels. Although presenting hotels on the screen in a list format seems appropriate for organizing the information, it creates a new (spurious) attribute for them: their position on the list. We tested experimentally whether the hotel’s position on the list affects its likelihood of being selected. Results revealed a nonlinear effect of hotel position on the list on choice: hotels that were listed at the top and bottom of the list were more likely to be chosen than those listed in the middle. This study suggests that even trivial web design choices, such as the choice of presenting data in lists, might result in nontrivial consequences on the behavior of prospective customers.

We report a hybrid mesoporous–planar architecture of methylammonium lead iodide perovskite based solar cells, to combine the benefits of both the mesoporous and planar architectures in a single device. A mesoporous-TiO2 grid was fabricated on a compact TiO2 layer, through a self-assembly process based on directional wetting, providing regions with and without mesoporous-TiO2, followed by perovskite deposition and back contact evaporation (hybrid cells). The hybrid cells showed up to 10.7% power conversion efficiency (PCE) as compared to 13.5% and 6.3% for their mesoporous and planar counterparts, respectively. Interestingly, the hybrid cells are found to show a short circuit current density(Jsc) as high as the Jsc of the mesoporous TiO2 based cells and proved to conserve the current density even in the absence of mesoporous-TiO2 from planar parts of the hybrid cells. The cells showed the best fill factor as compared to their mesoporous and planar counterparts. The areal variation in the meso to planar ratio has also been realized by changing the grid size to demonstrate the effect of the architecture on the cell performance. Charge extraction measurements have been used to obtain insight into the recombination inside different solar cells architectures. The hybrid cell structure emerged as a novel promising design for perovskite solar cells.

Serotonin leads to reduced food intake and satiety. Disrupted circadian rhythms lead to hyperphagia and obesity. The serotonergic and circadian systems are intertwined, as the central brain clock receives direct serotonergic innervation and, in turn, makes polysynaptic output back to serotonergic nuclei. Our objective was to test the hypothesis that peripherally serotonin alters circadian rhythms leading to a shift towards fat synthesis and weight gain. We studied the effect of serotonin and fluvoxamine, a selective serotonin reuptake inhibitor (SSRI), on the circadian clock and metabolic gene and protein expression in mouse liver, muscle and white adipose tissue (WAT) and cell culture. We found that serotonin and/or the SSRI fluvoxamine led to fat accumulation in mouse liver and hepatocytes by shifting metabolism towards fatty acid synthesis mainly through low average levels of phosphorylated acetyl CoA carboxylase (pACC) and phosphorylated protein phosphatase 2A (pPP2A). This shift towards fat synthesis was also observed in adipose tissue. Muscle cells were only slightly affected metabolically by serotonin or fluvoxamine. In conclusion, although centrally it leads to increased satiety, in peripheral tissues, such as the liver and WAT, serotonin induces fat accumulation.

Methionine is an essential sulfur amino acid that is engaged in key cellular functions such as protein synthesis and is a precursor for critical metabolites involved in maintaining cellular homeostasis. In mammals, in response to nutrient conditions, the liver plays a significant role in regulating methionine concentrations by altering its flux through the transmethylation, transsulfuration, and transamination metabolic pathways. A comprehensive understanding of how hepatic methionine metabolism intersects with other regulatory nutrient signaling and transcriptional events is, however, lacking. Here, we show that methionine and derived-sulfur metabolites in the transamination pathway activate the GCN5 acetyltransferase promoting acetylation of the transcriptional coactivator PGC-1alpha to control hepatic gluconeogenesis. Methionine was the only essential amino acid that rapidly induced PGC-1alpha acetylation through activating the GCN5 acetyltransferase. Experiments employing metabolic pathway intermediates revealed that methionine transamination, and not the transmethylation or transsulfuration pathways, contributed to methionine-induced PGC-1alpha acetylation. Moreover, aminooxyacetic acid, a transaminase inhibitor, was able to potently suppress PGC-1alpha acetylation stimulated by methionine, which was accompanied by predicted alterations in PGC-1alpha-mediated gluconeogenic gene expression and glucose production in primary murine hepatocytes. Methionine administration in mice likewise induced hepatic PGC-1alpha acetylation, suppressed the gluconeogenic gene program, and lowered glycemia, indicating that a similar phenomenon occurs in vivo These results highlight a communication between methionine metabolism and PGC-1alpha-mediated hepatic gluconeogenesis, suggesting that influencing methionine metabolic flux has the potential to be therapeutically exploited for diabetes treatment.

Methionine is an essential sulfur amino acid that is engaged in key cellular functions such as protein synthesis and is a precursor for critical metabolites involved in maintaining cellular homeostasis. In mammals, in response to nutrient conditions, the liver plays a significant role in regulating methionine concentrations by altering its flux through the transmethylation, transsulfuration, and transamination metabolic pathways. A comprehensive understanding of how hepatic methionine metabolism intersects with other regulatory nutrient signaling and transcriptional events is, however, lacking. Here, we show that methionine and derived-sulfur metabolites in the transamination pathway activate the GCN5 acetyltransferase promoting acetylation of the transcriptional coactivator PGC-1α to control hepatic gluconeogenesis. Methionine was the only essential amino acid that rapidly induced PGC-1α acetylation through activating the GCN5 acetyltransferase. Experiments employing metabolic pathway intermediates revealed that methionine transamination, and not the transmethylation or transsulfuration pathways, contributed to methionine-induced PGC-1α acetylation. Moreover, aminooxyacetic acid, a transaminase inhibitor, was able to potently suppress PGC-1α acetylation stimulated by methionine, which was accompanied by predicted alterations in PGC-1α-mediated gluconeogenic gene expression and glucose production in primary murine hepatocytes. Methionine administration in mice likewise induced hepatic PGC-1α acetylation, suppressed the gluconeogenic gene program, and lowered glycemia, indicating that a similar phenomenon occurs in vivo These results highlight a communication between methionine metabolism and PGC-1α-mediated hepatic gluconeogenesis, suggesting that influencing methionine metabolic flux has the potential to be therapeutically exploited for diabetes treatment.