The onset of leukaemia caused by type C retroviruses (MLV) in mice is accelerated by the emergence of recombinant polytropic or mink cell focus-forming (MCF) viruses. Susceptibility to infection by polytropic/MCF and also by closely related xenotropic MLV has been mapped to Rmc1 on mouse chromosome 1 (refs 5-7). To identify this gene, we introduced an expression cDNA library prepared from mouse NIH3T3 fibroblasts into nonpermissive hamster cells and screened these cells for acquired susceptibility to MCF viruses encoding beta-galactosidase and G418 resistance. From hamster cell clones identified in the screen, we recovered a mouse cDNA that maps to Rmc1 and confers MCF MLV infection when expressed in nonpermissive cell lines. It encodes a membrane protein related to Syg1p (suppressor of yeast G alpha deletion; ref. 8). The receptor-binding domain of the MCF MLV envelope protein binds specifically to Xenopus laevis oocytes that express mouse Syg1, suggesting it functions as a receptor that mediates virus entry. We also obtained the cDNA encoding human SYG1. When expressed in hamster cells, it establishes infectivity by MCF MLV as well as xenotropic MLV, which do not infect laboratory mice.

Understanding the role played by solid surfaces in ice nucleation is a significant step toward designing anti-icing surfaces. However, the uncontrollable impurities in water and surface heterogeneities remain a great challenge for elucidating the effects of surfaces on ice nucleation. Via a designed process of evaporation, condensation, and subsequent ice formation in a closed cell, we investigate the ice nucleation of ensembles of condensed water microdroplets on flat, solid surfaces with completely different wettabilities. The water microdroplets formed on flat, solid surfaces by an evaporation and condensation process exclude the uncontrollable impurities in water, and the effects of surface heterogeneities can be minimized through studying the freezing of ensembles of separate and independent water microdroplets. It is found that the normalized surface ice nucleation rate on a hydrophilic surface is about 1 order of magnitude lower than that on a hydrophobic surface. This is ascribed to the difference in the viscosity of interfacial water and the surface roughness.

Acute kidney injury (AKI) has been widely recognized as an important risk factor for the occurrence and development of chronic kidney disease (CKD). Even milder AKI has adverse consequences and could progress to renal fibrosis, which is the ultimate common pathway for various terminal kidney diseases. Thus, it is urgent to develop a strategy to hinder the transition from AKI to CKD. Some molecular mechanisms of AKI to CKD transition have been revealed, such as nephron loss, cell cycle arrest, persistent inflammation, endothelial injury with vascular rarefaction and epigenetic changes. Previous studies have elucidated the pivotal role of mitochondria in acute injuries and demonstrated that the fitness of this organelle is a major determinant in both the pathogenesis and recovery of organ function. Recent research has suggested that damage to mitochondrial function in early AKI is a crucial factor leading to tubular injury and persistent renal insufficiency. Dysregulation of mitochondrial homeostasis, alterations in bioenergetics, and organelle stress crosstalk contribute to the AKI to CKD transition. In this review, we focus on the pathophysiology of mitochondria in renal recovery after AKI and progression to CKD, confirming that targeting mitochondria represents a potentially effective therapeutic strategy for the progression of AKI to CKD.

Candida albicans biofilm infections are usually treated with azole antifungals such as fluconazole. However, the development of resistance to this drug in C. albicans biofilms is very common, especially in immunocompromised individuals. The upregulation of the sterol biosynthetic pathway gene ERG and the efflux pump genes CDR and MDR may contribute to this azole tolerance in Candida species. We hypothesize that farnesol, an endogenous quorum sensing molecule with possible antimicrobial properties which is also the precursor of ergosterols in C. albicans, may interfere with the development of fluconazole resistance in C. albicans biofilms. To test this hypothesis, MICs were compared and morphology changes were observed by confocal laser scanning microscopy (CLSM) for farnesol-treated and -untreated and fluconazole-resistant groups. The expression of possible target genes (ERG11, ERG25, ERG6, ERG5, ERG3, ERG1, MDR1, CDR1, and CDR2) in biofilms was analyzed by reverse transcription-PCR (RT-PCR) and quantitative PCR (qPCR) to investigate the molecular mechanisms of the inhibitory effects of farnesol. The results showed a decreased MIC of fluconazole and thinner biofilms for the farnesol-treated group, indicating that farnesol inhibited the development of fluconazole resistance. The sterol biosynthetic pathway may contribute to the inhibitory effects of farnesol, as the transcription levels of the ERG11, ERG25, ERG6, ERG3, and ERG1 genes decreased in the farnesol-treated group.

We report the electronic spectrum of the prototypical ruthenium coordination complex Ru(bpy)3 (2+) (bpy = 2, 2'-bipyridine) by messenger tagging with N2 in a cryogenic ion trap and photodissociation spectroscopy of mass selected Ru(bpy)3 (2+) ⋅ N2 ions. We observe individual electronic bands and groups of bands with unprecedented detail, particularly in the usually unresolved metal-to-ligand charge transfer region of the spectrum. By comparing our experimental results with time-dependent density functional theory, both with and without spin-orbit interaction [Heully et al., J. Chem. Phys. 131, 184308 (2009)], we are able to assign the spectrum of the isolated ion.

Unveiling the mystery of the contribution of nonsurface or noninterface sites in a catalyst to its catalytic performance remains a great challenge because of the difficulty in capturing precisely structural information (surface plus inner) encoded in the catalyst. This work attempts to elucidate the critical role of the internal vacancy in an atomically precise 24-atom gold cluster in regulating the catalytic performance on the hydrogenation reaction of CO 2 . The experiment results show that the Au 24 cluster with internal vacancy can mitigate sintering and exhibit high catalytic activity under relatively harsh reaction conditions, in contrast to the structurally similar Au 25 cluster without internal vacancy. Our computational study suggests that the internal vacancy in Au 24 provides the cluster with much more structural flexibility, which may be crucial to resisting the aggregation of the cluster and further postponing the deactivation. The hydrogenation and coupling stages of the reaction intermediates are proposed to explain the potential reaction pathway of CO 2 with H 2 on the Au 24 catalyst with internal vacancy.

We present photodissociation spectroscopy and computational analysis of three monocationic Cu-bipyridine complexes with one additional ligand of different interaction strength (N2, H2O and Cl) in the visible and UV. All three complexes show similar ππ* bands with origins slightly above 4 eV and vibrational band contours that are due to bipyridine ring deformation modes. Experiments at low temperature show that excited-state lifetime is the limiting factor for the width of the vibrational features. In the case of Cl as a ligand, there is a lower lying bright ligand-to-ligand charge-transfer state around 2.75 eV. The assignment of the transitions was made based on equation-of-motion coupled-cluster calculations. While the nature of the ligand does not significantly change the position of the bright ππ* state, it drastically changes the excited-state dynamics.

By using PBD and CCD, we obtained the optimal composition for xylanase production by Aspergillus niger XY-1 in SSF, and the results of no additional expensive medium and shortened fermentation time for higher xylanase production show the potential for industrial utilization.