We present the pressure area isotherms for Langmuir films made of calix[8]arene, the calix[8]arene/C60 complex, and the calix[8]arene/C70 complex, all of them measured at 306.1 K. A Brewster angle microscope was used to observe the phases shown by the π−A isotherms. In these three cases, we found a solid phase and its solid−gas coexistence but no expanded liquid phases. The Langmuir films made of calix[8]arene and the calix[8]arene/C60 complex are very similar. The experimental information is consistent with the assumption that C60 is situated inside the cavity of calix[8]arene. The Langmuir films of calix[8]arene and the calix[8]arene/C70 complex are not very similar; we present a discussion to explain the origin of this difference.

Mammalian class I aldehyde dehydrogenase (ALDH) plays an important role in the biosynthesis of the hormone retinoic acid (RA), which modulates gene expression and cell differentiation. RA has been shown to mediate control of human ALDH1 gene expression through modulation of the retinoic acid receptor α (RARα) and the CCAAT/enhancer binding protein β (C/EBPβ). The positive activation of these transcription factors on the ALDH1 promoter is inhibited by RA through a decrease of C/EBPβ binding to the ALDH1 CCAAT box response element. However, the mechanism of this effect remains unknown. Here we report that the RARα/retinoid X receptor β (RXRβ) complex binds to the mouse retinaldehyde dehydrogenase 1 (Raldh1) promoter at a non-consensus RA response element (RARE) with similar affinity to that of the consensus RARE. We found that C/EBPβ binds to a Raldh1 CCAAT box located at -82/-58 bp, adjacent to the RARE. Treatment with RA increases GADD153 and GADD153-C/EBPβ interaction resulting in a decreased cellular availability of C/ EBPβ for binding to the Raldh1 CCAAT box. These data support a model in which high RA levels inhibit Raldh1 gene expression by sequestering C/EBPβ through its interaction to GADD153.

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The genomic sequences of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) worldwide are publicly available and are derived from studies due to the increase in the number of cases. The importance of study of mutations is related to the possible virulence and diagnosis of SARS‐CoV‐2. To identify circulating mutations present in SARS‐CoV‐2 genomic sequences in Mexico, Belize, and Guatemala to find out if the same strain spread to the south, and analyze the specificity of the primers used for diagnosis in these samples. Twenty three complete SARS‐CoV‐2 genomic sequences, available in the GISAID database from May 8 to September 11, 2020 were analyzed and aligned versus the genomic sequence reported in Wuhan, China (NC_045512.2), using Clustal Omega. Open reading frames were translated using the ExPASy Translate Tool and UCSF Chimera (v.1.12) for amino acid substitutions analysis. Finally, the sequences were aligned versus primers used in the diagnosis of COVID‐19. One hundred and eighty seven distinct variants were identified, of which 102 are missense, 66 synonymous and 19 noncoding. P4715L and P5828L substitutions in replicase polyprotein were found, as well as D614G in spike protein and L84S in ORF8 in Mexico, Belize, and Guatemala. The primers design by CDC of United States showed a positive E value. The genomic sequences of SARS‐CoV‐2 in Mexico, Belize, and Guatemala present similar mutations related to a virulent strain of greater infectivity, which could mean a greater capacity for inclusion in the host genome and be related to an increased spread of the virus in these countries, furthermore, its diagnosis would be affected.

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