Metal-Dependent and Selective Crystallization of CAU-10 and MIL-53 Frameworks through Linker Nitration

The reaction of the V-shaped linker molecule 5-hydroxyisophthalic acid (H2 L0 ), with Al or Ga nitrate under almost identical reaction conditions leads to the nitration of the linker and subsequent formation of metal-organic frameworks (MOFs) with CAU-10 or MIL-53 type structure of composition [Al(OH)(L)], denoted as Al-CAU-10-L0, 2, 4, 6 or [Ga(OH)(L)], denoted as Ga-MIL-53-L2 . The Al-MOF contains the original linker L0 as well as three different nitration products (L2 , L4 and L4/6 ), whereas the Ga-MOF mainly incorporates the linker L2 . The compositions were deduced by 1 H NMR spectroscopy and confirmed by Rietveld refinement. In situ and ex situ studies were carried out to follow the nitration and crystallization, as well as the composition of the MOFs. The crystal structures were refined against powder X-ray diffraction (PXRD) data. As anticipated, the use of the V-shaped linker results in the formation of the CAU-10 type structure in the Al-MOF. Unexpectedly, the Ga-MOF crystallizes in a MIL-53 type structure, which is usually observed with linear or slightly bent linker molecules. To study the structure directing effect of the in situ nitrated linker, pure 2-nitrobenzene-1,3-dicarboxylic acid (m-H2 BDC-NO2 ) was employed which exclusively led to the formation of [Ga(OH)(C8 H3 NO6 )] (Ga-MIL-53-m-BDC-NO2 ), which is isoreticular to Ga-MIL-53-L2 . Density Functional Theory (DFT) calculations confirmed the higher stability of Ga-MIL-53-L2 compared to Ga-CAU-10-L2 and grand canonical Monte Carlo simulations (GCMC) are in agreement with the observed water adsorption isotherms of Ga-MIL-53-L2

How society’s negative view of videogames can discourage brands from sponsoring eSports

The purpose of this research was to identify the main motives that contribute to society’s negative view of videogames and that present a risk to the eSports sponsors’ image. To achieve this, an exploratory, qualitative, and integrative literature review was conducted. According to the theoretical data, there are four main reasons why society has a negative perception of videogames. It is commonly believed that: (1) gaming is an unproductive activity, (2) violent videogames incite aggressive behaviors, (3) videogames lead to gaming-addiction, and (4) eSports lead to eSports-related gambling addiction. However, while the literature presents convincing evidence that gaming can create addiction and that eSports can promote gambling addiction, there is no conclusive evidence to assume that violent videogames lead to aggressiveness and there is evidence showing that playing videogames can be a productive activity. Nevertheless, these four beliefs are a threat to the eSports sponsors’ image and may lead them to cancel their existing sponsorships or lead other brands to not want to sponsor eSports to prevent being associated with these negative notions. This research will help expand the minor literature on eSports sponsorships and advance the knowledge of why some eSports sponsorships are terminated and why some brands may be reluctant to sponsor eSports.info:eu-repo/semantics/publishedVersio

The archaeal proteasome is regulated by a network of AAA ATPases

The proteasome is the central machinery for targeted protein degradation in archaea, Actinobacteria, and eukaryotes. In its basic form, it consists of a regulatory ATPase complex and a proteolytic core particle. The interaction between the two is governed by an HbYX motif (where Hb is a hydrophobic residue, Y is tyrosine, and X is any amino acid) at the C terminus of the ATPase subunits, which stimulates gate opening of the proteasomal α-subunits. In archaea, the proteasome-interacting motif is not only found in canonical proteasome-activating nucleotidases of the PAN/ARC/Rpt group, which are absent in major archaeal lineages, but also in proteins of the CDC48/p97/VAT and AMA groups, suggesting a regulatory network of proteasomal ATPases. Indeed, Thermoplasma acidophilum, which lacks PAN, encodes one CDC48 protein that interacts with the 20S proteasome and activates the degradation of model substrates. In contrast, Methanosarcina mazei contains seven AAA proteins, five of which, both PAN proteins, two out of three CDC48 proteins, and the AMA protein, function as proteasomal gatekeepers. The prevalent presence of multiple, distinct proteasomal ATPases in archaea thus results in a network of regulatory ATPases that may widen the substrate spectrum of proteasomal protein degradation

Tropical Pacific climate and its response to global warming in the Kiel climate model.

A new, non-flux corrected, global climate model is introduced, the Kiel Climate Model (KCM), which will be used to study internal climate variability from interannual to millennial time scales and climate predictability of the first and second kind. The version described here is a coarse resolution version that will be employed in extended-range integrations of several millennia. KCM's performance in the Tropical Pacific with respect to mean state, annual cycle, and El Niño/Southern Oscillation (ENSO) is described. Additionally, the Tropical Pacific response to global warming is studied.Overall, climate drift in a multi-century control integration is small. However, KCM exhibits an equatorial cold bias at the surface of the order 1°C, while strong warm biases of several degrees are simulated in the eastern Tropical Pacific on both sides off the equator, with maxima near the coasts. The annual and semi-annual cycles are realistically simulated in the eastern and western equatorial Pacific, respectively. ENSO performance compares favorably to observations with respect to both amplitude and period.An ensemble of eight greenhouse warming simulations was performed, in which the CO2 concentration was increased by 1% per year until doubling was reached, and stabilized thereafter. Warming of equatorial Pacific sea surface temperature (SST) is, to first order, zonally symmetric and leads to a sharpening of the thermocline. ENSO variability increases due to global warming: During the 30 year period after CO2 doubling, the ensemble mean standard deviation of Niño3 SST anomalies is increased by 26% relative to the control, and power in the ENSO band is almost doubled. The increased variability is due to both a strengthened (22%) thermocline feedback and an enhanced (52%) atmospheric sensitivity to SST, both are associated with changes in the basic state. Although variability increases in the mean, there is a large spread among ensemble members and hence a finite probability that in the “model world” no change in ENSO would be observed.<br/

Structure-Function Analysis of the Human JC Polyomavirus Establishes the LSTc Pentasaccharide as a Functional Receptor Motif

SummaryThe human JC polyomavirus (JCV) causes a fatal demyelinating disease, progressive multifocal leukoencephalopathy (PML), in immunocompromised individuals. Current treatment options for PML are inadequate. Sialylated oligosaccharides and the serotonin receptor are known to be necessary for JCV entry, but the molecular interactions underlying JCV attachment remain unknown. Using glycan array screening and viral infectivity assays, we identify a linear sialylated pentasaccharide with the sequence NeuNAc-α2,6-Gal-β1,4-GlcNAc-β1,3-Gal-β1,4-Glc (LSTc) present on host glycoproteins and glycolipids as a specific JCV recognition motif. The crystal structure of the JCV capsid protein VP1 was solved alone and in complex with LSTc. It reveals extensive interactions with the terminal sialic acid of the LSTc motif and specific recognition of an extended conformation of LSTc. Mutations in the JCV oligosaccharide-binding sites abolish cell attachment, viral spread, and infectivity, further validating the importance of this interaction. Our findings provide a powerful platform for the development of antiviral compounds

A structure-guided mutation in the major capsid protein retargets BK polyomavirus.

Viruses within a family often vary in their cellular tropism and pathogenicity. In many cases, these variations are due to viruses switching their specificity from one cell surface receptor to another. The structural requirements that underlie such receptor switching are not well understood especially for carbohydrate-binding viruses, as methods capable of structure-specificity studies are only relatively recently being developed for carbohydrates. We have characterized the receptor specificity, structure and infectivity of the human polyomavirus BKPyV, the causative agent of polyomavirus-associated nephropathy, and uncover a molecular switch for binding different carbohydrate receptors. We show that the b-series gangliosides GD3, GD2, GD1b and GT1b all can serve as receptors for BKPyV. The crystal structure of the BKPyV capsid protein VP1 in complex with GD3 reveals contacts with two sialic acid moieties in the receptor, providing a basis for the observed specificity. Comparison with the structure of simian virus 40 (SV40) VP1 bound to ganglioside GM1 identifies the amino acid at position 68 as a determinant of specificity. Mutation of this residue from lysine in BKPyV to serine in SV40 switches the receptor specificity of BKPyV from GD3 to GM1 both in vitro and in cell culture. Our findings highlight the plasticity of viral receptor binding sites and form a template to retarget viruses to different receptors and cell types