Bradypehrson2585

The synthesis of solid acids with strong zeolite-like acidity and textural properties like amorphous aluminosilicates (ASAs) is still a challenge. In this work, we report the synthesis of amorphous "acidic aluminosilicates (AAS)", which possesses Brønsted acidic sites like in zeolites and textural properties like ASAs. AAS catalyzes different reactions (styrene oxide ring-opening, vesidryl synthesis, Friedel-Crafts alkylation, jasminaldehyde synthesis, m-xylene isomerization, and cumene cracking) with better performance than state-of-the-art zeolites and amorphous aluminosilicates. Notably, AAS efficiently converts a range of waste plastics to hydrocarbons at significantly lower temperatures. A Cu-Zn-Al/AAS hybrid shows excellent performance for CO2 to fuel conversion with 79% selectivity for dimethyl ether. Conventional and DNP-enhanced solid-state NMR provides a molecular-level understanding of the distinctive Brønsted acidic sites of these materials. Due to their unique combination of strong acidity and accessibility, AAS will be a potential alternative to zeolites.Cells in biofilms dynamically adapt to surrounding environmental conditions, which alters biofilm architecture. The obligate anaerobic pathogen Clostridium perfringens shows different biofilm structures in different temperatures. Here we find that the temperature-regulated production of extracellular polymeric substance (EPS) is necessary for morphological changes in biofilms. We identify BsaA proteins as an EPS matrix necessary for pellicle biofilm formation at lower temperature and find that extracellularly secreted BsaA protein forms filamentous polymers. We show that sipW-bsaA operon expression is bimodal, and the EPS-producing population size is increased at a lower temperature. This heterogeneous expression of the EPS gene requires a two-component system. We find that EPS-producing cells cover EPS-nonproducing cells attaching to the bottom surface. In the deletion mutant of pilA2, encoding a type IV pilin, the EPS gene expression is ON in the whole population. This heterogeneity is further regulated by the cleavage of the pilA2 mRNA by RNase Y, causing temperature-responsive EPS expression in biofilms. As temperature is an environmental cue, C. perfringens may modulate EPS expression to induce morphological changes in biofilm structure as a strategy for adapting to interhost and external environments.The deregulated genes in colorectal cancer (CRC) vary significantly across different studies. Thus, a systems biology approach is needed to identify the co-deregulated genes (co-DEGs), explore their molecular networks, and spot the major hub proteins within these networks. We reanalyzed 19 GEO gene expression profiles to identify and annotate CRC versus normal signatures, single-gene perturbation, and single-drug perturbation signatures. We identified the co-DEGs across different studies, their upstream regulating kinases and transcription factors (TFs). Connectivity Map was used to identify likely repurposing drugs against CRC within each group. The functional changes of the co-upregulated genes in the first category were mainly associated with negative regulation of transforming growth factor β production and glomerular epithelial cell differentiation; whereas the co-downregulated genes were enriched in cotranslational protein targeting to the membrane. We identified 17 hub proteins across the co-upregulated genes and 18 hub proteins across the co-downregulated genes, composed of well-known TFs (MYC, TCF3, PML) and kinases (CSNK2A1, CDK1/4, MAPK14), and validated most of them using GEPIA2 and HPA, but also through two signature gene lists composed of the co-up and co-downregulated genes. Selleck Darovasertib We further identified a list of repurposing drugs that can potentially target the co-DEGs in CRC, including camptothecin, neostigmine bromide, emetine, remoxipride, cephaeline, thioridazine, and omeprazole. Similar analyses were performed in the co-DEG signatures in single-gene or drug perturbation experiments in CRC. MYC, PML, CDKs, CSNK2A1, and MAPKs were common hub proteins among all studies. Overall, we identified the critical genes in CRC and we propose repurposing drugs that could be used against them.Fermi liquids (FLs) display a quadratic temperature (T) dependent resistivity. This can be caused by electron-electron (e-e) scattering in presence of inter-band or Umklapp scattering. However, dilute metallic SrTiO3 was found to display T2 resistivity in absence of either of the two mechanisms. The presence of soft phonons as possible scattering centers raised the suspicion that T2 resistivity is not due to e-e scattering. Here, we present the case of Bi2O2Se, a layered semiconductor with hard phonons, which becomes a dilute metal with a small single-component Fermi surface upon doping. It displays T2 resistivity well below the degeneracy temperature in absence of Umklapp and inter-band scattering. We observe a universal scaling between the T2 resistivity prefactor (A) and the Fermi energy (EF), an extension of the Kadowaki-Woods plot to dilute metals. Our results imply the absence of a satisfactory understanding of the ubiquity of e-e T2 resistivity in FLs.Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr Virus (EBV) establish life-long infections and are associated with malignancies. Striking geographic variation in incidence and the fact that virus alone is insufficient to cause disease, suggests other co-factors are involved. Here we present epidemiological analysis and genome-wide association study (GWAS) in 4365 individuals from an African population cohort, to assess the influence of host genetic and non-genetic factors on virus antibody responses. EBV/KSHV co-infection (OR = 5.71(1.58-7.12)), HIV positivity (OR = 2.22(1.32-3.73)) and living in a more rural area (OR = 1.38(1.01-1.89)) are strongly associated with immunogenicity. GWAS reveals associations with KSHV antibody response in the HLA-B/C region (p = 6.64 × 10-09). For EBV, associations are identified for VCA (rs71542439, p = 1.15 × 10-12). Human leucocyte antigen (HLA) and trans-ancestry fine-mapping substantiate that distinct variants in HLA-DQA1 (p = 5.24 × 10-44) are driving associations for EBNA-1 in Africa.