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A bstract We study the physical mechanism of how an external magnetic field influences the QCD quark condensate. Two competing mechanisms are identified, both relying on the interaction between the magnetic field and the low quark modes. While the coupling to valence quarks enhances the condensate, the interaction with sea quarks suppresses it in the transition region. The latter “sea effect” acts by ordering the Polyakov loop and, thereby, reduces the number of small Dirac eigenmodes and the condensate. It is most effective around the transition temperature, where the Polyakov loop effective potential is flat and a small correction to it by the magnetic field can have a significant effect. Around the critical temperature, the sea suppression overwhelms the valence enhancement, resulting in a net suppression of the condensate, named inverse magnetic catalysis. We support this physical picture by lattice simulations including continuum extrapolated results on the Polyakov loop as a function of temperature and magnetic field. We argue that taking into account the increase in the Polyakov loop and its interaction with the low-lying modes is essential to obtain the full physical picture, and should be incorporated in effective models for the description of QCD in magnetic fields in the transition region.

A bstract We study the problems of chiral symmetry breaking and eigenmode localisation in finite-temperature QCD by looking at the lattice Dirac operator as a random Hamiltonian. We recast the staggered Dirac operator into an unconventional three-dimensional Anderson Hamiltonian (“Dirac-Anderson Hamiltonian”) carrying internal degrees of freedom, with disorder provided by the fluctuations of the gauge links. In this framework, we identify the features relevant to chiral symmetry restoration and localisation of the low-lying Dirac eigenmodes in the ordering of the local Polyakov lines, and in the related correlation between spatial links across time slices, thus tying the two phenomena to the deconfinement transition. We then build a toy model based on QCD and on the Dirac-Anderson approach, replacing the Polyakov lines with spin variables and simplifying the dynamics of the spatial gauge links, but preserving the above-mentioned relevant dynamical features. Our toy model successfully reproduces the main features of the QCD spectrum and of the Dirac eigenmodes concerning chiral symmetry breaking and localisation, both in the ordered (deconfined) and disordered (confined) phases. Moreover, it allows us to study separately the roles played in the two phenomena by the diagonal and the off-diagonal terms of the Dirac-Anderson Hamiltonian. Our results support our expectation that chiral symmetry restoration and localisation of the low modes are closely related, and that both are triggered by the deconfinement transition.

Environmental biotechnology offers several promising techniques for the rehabilitation of polluted environments. The modern industrialized world presents novel challenges to the environmental sciences, requiring a constant development and deepening of knowledge to enable the characterization of novel pollutants and a better understanding of the bioremediation strategies as well as their limiting factors. The success of bioremediation depends heavily on the survival and activities of indigenous microbial communities and their interaction with introduced microorganisms. The majority of natural microbiomes remain uncultivated; therefore, further investigations focusing on their intrinsic functions in ecosystems are needed. In this review, we aimed to provide (a) a comprehensive overview of the presence of viable but nonculturable bacteria and yet-to-be-cultivated cells in nature and their diverse awakening strategies in response to, among other factors, signalling extracellular metabolites (autoinducers, resuscitation promoting factors, and siderophores); (b) an outline of the trends in isolating unculturable bacteria; and (c) the potential applications of these hidden players in rehabilitation processes.

Gonadal hormone 17β-estradiol (E2) and its receptors are key regulators of gene transcription by binding to estrogen responsive elements in the genome. Besides the classical genomic action, E2 regulates gene transcription via the modification of epigenetic marks on DNA and histone proteins. Depending on the reaction partner, liganded estrogen receptor (ER) promotes DNA methylation at the promoter or enhancer regions. In addition, ERs are important regulators of passive and active DNA demethylation. Furthermore, ERs cooperating with different histone modifying enzymes and chromatin remodeling complexes alter gene transcription. In this review, we survey the basic mechanisms and interactions between estrogen receptors and DNA methylation, demethylation and histone modification processes as well as chromatin remodeling complexes. The particular relevance of these mechanisms to physiological processes in memory formation, embryonic development, spermatogenesis and aging as well as in pathophysiological changes in carcinogenesis is also discussed.

We recently obtained an estimate of the axion mass based on the hypothesis that axions make up most of the dark matter in the universe. A key ingredient for this calculation was the temperature-dependence of the topological susceptibility of full QCD. Here we summarize the calculation of the susceptibility in a range of temperatures from well below the finite temperature cross-over to around 2 GeV. The two main difficulties of the calculation are the unexpectedly slow convergence of the susceptibility to its continuum limit and the poor sampling of nonzero topological sectors at high temperature. We discuss how these problems can be solved by two new techniques, the first one with reweighting using the quark zero modes and the second one with the integration method.

Interleukin-1β (IL-1β) is a key mediator of non-alcoholic steatohepatitis (NASH), a chronic liver disease, and of systemic inflammation-driven aging. IL-1β contributes to cardio-metabolic decline, and may promote hepatic oncogenic transformation. Therefore, IL-1β is a potential therapeutic target in these pathologies. We aimed to investigate the hepatic and cardiac effects of an IL-1β targeting monoclonal antibody in an aged mouse model of NASH. 24 months old male C57Bl/6J mice were fed with control or choline deficient (CDAA) diet and were treated with isotype control or anti-IL-1β Mab for 8 weeks. Cardiac functions were assessed by conventional—and 2D speckle tracking echocardiography. Liver samples were analyzed by immunohistochemistry and qRT-PCR. Echocardiography revealed improved cardiac diastolic function in anti-IL-1β treated mice with NASH. Marked hepatic fibrosis developed in CDAA-fed group, but IL-1β inhibition affected fibrosis only at transcriptomic level. Hepatic inflammation was not affected by the IL-1β inhibitor. PCNA staining revealed intensive hepatocyte proliferation in CDAA-fed animals, which was not influenced by neutralization of IL-1β. IL-1β inhibition increased hepatic expression of Pd-1 and Ctla4 , while Pd-l1 expression increased in NASH. In conclusion, IL-1β inhibition improved cardiac diastolic function, but did not ameliorate features of NASH; moreover, even promoted hepatic immune checkpoint expression, with concomitant NASH-related hepatocellular proliferation.

Hierarchical functionalisation of the UiO-66(Zr)-NH2 metal–organic framework with cysteine, poly(ethylene glycol) (PEG), and the SARS-CoV-2 spike receptor-binding domain (RBD) was developed to enable receptor-specific interaction with the angiotensin-converting enzyme 2 receptor (ACE2) in model cells. Post-synthetic modification using cysteine and heterobifunctional PEG linkers allowed controlled bioconjugation of SpyTag-labelled RBD via SpyTag/SpyCatcher chemistry, while preserving the crystallinity, microporosity, and intrinsic optical properties of the UiO-66(Zr)-NH2 framework. Comprehensive physicochemical characterisation confirmed successful surface functionalisation, tunable aggregation behaviour, and retention of multimodal optical characteristics. Cellular studies in HEK293T and HeLa cells overexpressing EGFP-tagged ACE2 demonstrated enhanced and selective association and uptake of RBD-functionalised nanoparticles compared with non-targeted analogues. Multimodal fluorescence imaging, fluorescence lifetime imaging microscopy, flow-cytometry, and electron microscopy indicated ACE2-dependent endocytic internalisation, with predominant localisation in endosomal and autophagosomal compartments, while both amine- and cysteine-modified formulations exhibited good biocompatibility. Overall, this study establishes a virus-mimetic, ACE2-targeted UiO-66(Zr)-based nanosystem as a proof-of-concept biointerface platform for receptor-specific cellular delivery and imaging, providing a foundation for future MOF-based nanocarriers exploiting ligand–receptor interactions.

The increasing incidence of carbapenemase-producing K. pneumoniae strains (CP-Kps) in the last decade has become a serious global healthcare problem. Therapeutic options for the treatment of emerging hospital clones have drastically narrowed and therefore novel approaches must be considered. Here we have isolated and characterized a lytic bacteriophage, named vB_KpnS_Kp13, that was effective against all Verona integron-encoded metallo-β-lactamase (VIM) producing K. pneumoniae isolates originating from hospital samples (urine, blood, sputum and faeces), belonging to the ST15 clonal lineage and expressing the K24 capsule. Morphological characterization of vB_KpnS_Kp13 showed that the newly identified phage belonged to the Siphoviridae family, and phylogenetic analysis showed that it is part of a distinct clade of the Tunavirinae subfamily. Functional analysis revealed that vB_KpnS_Kp13 had relatively short latent period times (18 minutes) compared to other K. pneumoniae bacteriophages and could degrade biofilm by more than 50% and 70% in 24 and 48 hours respectively. Complete in vivo rescue potential of the new phage was revealed in an intraperitoneal mouse model where phages were administered intraperitoneally 10 minutes after bacterial challenge. Our findings could potentially be used to develop specific anti-CP-Kps bacteriophage-based therapeutic strategies against major clonal lineages and serotypes.

It is by now well established that Dirac fermions coupled to non-Abelian gauge theories can undergo an Anderson-type localization transition. This transition affects eigenmodes in the lowest part of the Dirac spectrum, the ones most relevant to the low-energy physics of these models. Here we review several aspects of this phenomenon, mostly using the tools of lattice gauge theory. In particular, we discuss how the transition is related to the finite-temperature transitions leading to the deconfinement of fermions, as well as to the restoration of chiral symmetry that is spontaneously broken at low temperature. Other topics we touch upon are the universality of the transition, and its connection to topological excitations (instantons) of the gauge field and the associated fermionic zero modes. While the main focus is on Quantum Chromodynamics, we also discuss how the localization transition appears in other related models with different fermionic contents (including the quenched approximation), gauge groups, and in different space-time dimensions. Finally, we offer some speculations about the physical relevance of the localization transition in these models.

Cyclodextrins, representing a versatile family of cyclic oligosaccharides, have extensive pharmaceutical applications due to their unique truncated cone-shaped structure with a hydrophilic outer surface and a hydrophobic cavity, which enables them to form non-covalent host–guest inclusion complexes in pharmaceutical formulations to enhance the solubility, stability and bioavailability of numerous drug molecules. As a result, cyclodextrins are mostly considered as inert carriers during their medical application, while their ability to interact not only with small molecules but also with lipids and proteins is largely neglected. By forming inclusion complexes with cholesterol, cyclodextrins deplete cholesterol from cellular membranes and thereby influence protein function indirectly through alterations in biophysical properties and lateral heterogeneity of bilayers. In this review, we summarize the general chemical principles of direct cyclodextrin–protein interactions and highlight, through relevant examples, how these interactions can modify protein functions in vivo, which, despite their huge potential, have been completely unexploited in therapy so far. Finally, we give a brief overview of disorders such as Niemann–Pick type C disease, atherosclerosis, Alzheimer’s and Parkinson’s disease, in which cyclodextrins already have or could have the potential to be active therapeutic agents due to their cholesterol-complexing or direct protein-targeting properties.