A new magnetic field dependence of Landau levels on a graphene like structure

We consider a tight-binding model on the honeycomb lattice in a magnetic field. For special values of the hopping integrals, the dispersion relation is linear in one direction and quadratic in the other. We find that, in this case, the energy of the Landau levels varies with the field B as E_n(B) ~ [(n+\gamma)B]^{2/3}. This result is obtained from the low-field study of the tight-binding spectrum on the honeycomb lattice in a magnetic field (Hofstadter spectrum) as well as from a calculation in the continuum approximation at low field. The latter links the new spectrum to the one of a modified quartic oscillator. The obtained value $\gamma=1/2$ is found to result from the cancellation of a Berry phase.Comment: 4 pages, 4 figure

Inducible Selectable Marker Genes to Improve Aspergillus fumigatus Genetic Manipulation

The hygromycin B phosphotransferase gene from Escherichia coli and the pyrithiamine resistance gene from Aspergillus oryzae are two dominant selectable marker genes widely used to genetically manipulate several fungal species. Despite the recent development of CRISPR/Cas9 and marker-free systems, in vitro molecular tools to study Aspergillus fumigatus, which is a saprophytic fungus causing life-threatening diseases in immunocompromised hosts, still rely extensively on the use of dominant selectable markers. The limited number of drug selectable markers is already a critical aspect, but the possibility that their introduction into a microorganism could induce enhanced virulence or undesired effects on metabolic behavior constitutes another problem. In this context, here, we demonstrate that the use of ptrA in A. fumigatus leads to the secretion of a compound that allows the recovery of thiamine auxotrophy. In this study, we developed a simple modification of the two commonly used dominant markers in which the development of resistance can be controlled by the xylose-inducible promoter PxylP from Penicillium chrysogenum. This strategy provides an easy solution to avoid undesired side effects, since the marker expression can be readily silenced when not required

Ligand-Assisted Gold-Catalyzed Efficient Alkynylative Cyclization with Terminal Alkynes Using H2O2 as Oxidant

The gold-catalyzed cyclization-functionalization is a powerful approach to construct high-value organic molecules. However, current strategies mainly rely on expensive external oxidants or pre-functionalized substrates, which exhibit low atom economy and high costs. Considering the current increasing demand for environmentally friendly and atomically efficient processes, the development of greener and more efficient synthetic strategies becomes more valuable and attractive. To circumvent these drawbacks, we developed a green gold-catalyzed cyclization-functionalization strategy using hydrogen peroxide as oxidant. A direct construction of 3-alkynylbenzofurans from terminal alkynes was possible by this gold-catalyzed process. Green and inexpensive oxidants, simple gold catalysts, mild reaction conditions, high atom economy, remarkable selectivity, wide substrate scope, broad functional group compatibility and a facile gram-scale synthesis make this alkynylative cyclization method practical for many forms of cyclization reactions. In contrast to prior methods neither pre-functionalized alkynes nor expensive external oxidants are needed

Experimental Heart Failure Induces Alterations of the Lung Proteome - Insight into Molecular Mechanisms

Background: Heart failure (CHF) is characterized by dyspnea and pulmonary changes. The underlying molecular adaptations are unclear, but might provide targets for therapeutic interventions. We therefore conceived a study to determine molecular changes of early pulmonary stress failure in a model of tachycardia-induced heart failure. Methods: CHF was induced in rabbits by progessive right ventricular pacing (n=6). Invasive blood pressure measurements and echocardiography were repeatedly performed. Untreated animals served as controls (n=6). Pulmonary tissue specimens were subjected to two-dimensional gel electrophoresis, and differentially expressed proteins were identified by mass spectrometry. Selected proteins were validated by Western Blot analysis and localized by immunohistochemical staining. Results: CHF animals were characterized by significantly altered functional, morphological, and hemodynamic parameters. Upon proteomic profiling, a total of 33 proteins was found to be differentially expressed in pulmonary tissue of CHF animals (18 up-regulated, and 15 down-regulated) belonging to 4 functional groups: 1. proteins involved in maintaining cytoarchitectural integrity, 2. plasma proteins indicating impaired alveolar-capillary permeability, 3. proteins with antioxidative properties, and 4. proteins participating in the metabolism of selenium compounds Conclusion: Experimental heart failure profoundly alters the pulmonary proteome. Our results supplement the current knowledge of pulmonary stress failure by specifying its molecular fundament

Metabolic imbalance of T cells in COVID-19 is hallmarked by basigin and mitigated by dexamethasone

Metabolic pathways regulate immune responses and disrupted metabolism leads to immune dysfunction and disease. Coronavirus disease 2019 (COVID-19) is driven by imbalanced immune responses, yet the role of immunometabolism in COVID-19 pathogenesis remains unclear. By investigating 87 patients with confirmed SARS-CoV-2 infection, 6 critically ill non–COVID-19 patients, and 47 uninfected controls, we found an immunometabolic dysregulation in patients with progressed COVID-19. Specifically, T cells, monocytes, and granulocytes exhibited increased mitochondrial mass, yet only T cells accumulated intracellular reactive oxygen species (ROS), were metabolically quiescent, and showed a disrupted mitochondrial architecture. During recovery, T cell ROS decreased to match the uninfected controls. Transcriptionally, T cells from severe/critical COVID-19 patients showed an induction of ROS-responsive genes as well as genes related to mitochondrial function and the basigin network. Basigin (CD147) ligands cyclophilin A and the SARS-CoV-2 spike protein triggered ROS production in T cells in vitro. In line with this, only PCR-positive patients showed increased ROS levels. Dexamethasone treatment resulted in a downregulation of ROS in vitro and T cells from dexamethasone-treated patients exhibited low ROS and basigin levels. This was reflected by changes in the transcriptional landscape. Our findings provide evidence of an immunometabolic dysregulation in COVID-19 that can be mitigated by dexamethasone treatment