It was recently found that the Lee-Huang-Yang (LHY) correction to the mean-field Hamiltonian of binary atomic boson condensates suppresses the collapse and creates stable localized modes (twocomponent "quantum droplets", QDs) in two and three dimensions (2D and 3D). In particular, the LHY effect modifies the effective Gross-Pitaevskii equation (GPE) in 2D by adding a logarithmic factor to the usual cubic term. In the framework of the accordingly modified two-component GPE system, we construct 2D self-trapped modes in the form of QDs with vorticity S embedded into each component. Due to the effect of the logarithmic factor, the QDs feature a flat-top shape, which expands with the increase of S and norm N . An essential finding, produced by a systematic numerical investigation and analytical estimates, is that the vortical QDs are stable (which is a critical issue for vortex solitons in nonlinear models) up to S = 5, for N exceeding a certain threshold value, which is predicted to scale as N th ∼ S 4 for large S (for three-dimensional QDs, the scaling is N th ∼ S 6 ). The prediction is corroborated by numerical findings. Pivots of QDs with S ≥ 2 are subject to structural instability, as specially selected perturbations can split the single pivot in a set of S or S + 2 pivots corresponding to unitary vortices; however, the structural instability remains virtually invisible, as it occurs in a broad central "hole" of the vortex soliton, where values of fields are very small, and it does not cause any dynamical instability. In the condensate of 39 K atoms, in which QDs with S = 0 and a quasi-2D shape were created recently, the vortical droplets may have radial size 30 µm, with the number of atoms in the range of 10 4 − 10 5 . The role of three-body losses is considered too, demonstrating that they do not prevent the creation of the vortex droplets, but may produce a noteworthy effect, leading to sudden splitting of "light" droplets. In addition, hidden-vorticity states in QDs, with topological charges S+ = −S− = 1 in their components, which are prone to strong instability in other settings, have their stability region too. Unstable HV states tend to spontaneously merge into zero-vorticity solitons. Collisions of QDs, which may lead to their merger, and dynamics of elliptically deformed QDs (which form rotating elongated patterns or ones with oscillations of the eccentricity) are briefly considered too.

We study two-dimensional (2D) matter-wave solitons in spinor Bose-Einstein condensates under the action of the spin-orbit coupling and opposite signs of the self-and cross-interactions. Stable 2D twocomponent solitons of the mixed-mode type are found if the cross-interaction between the components is attractive, while the self-interaction is repulsive in each component. Stable solitons of the semi-vortex type are formed in the opposite case, under the action of competing self-attraction and cross-repulsion. The solitons exist with the total norm taking values below a collapse threshold. Further, in the case of the repulsive self-interaction and inter-component attraction, stable 2D selftrapped modes, which may be considered as quantum droplets (QDs), are created if the beyondmean-field Lee-Huang-Yang terms are added to the self-repulsion in the underlying system of coupled Gross-Pitaevskii equations. Stable QDs of the mixed-mode type, of a large size with an anisotropic density profile, exist with arbitrarily large values of the norm, as the Lee-Huang-Yang terms eliminate the collapse. The effect of the spin-orbit coupling term on characteristics of the QDs is systematically studied. We also address the existence and stability of QDs in the case of SOC with mixed Rashba and Dresselhaus terms, which makes the density profile of the QD more isotropic. Thus, QDs in the spin-orbit-coupled binary Bose-Einstein condensate are for the first time studied in the present work.

Aberrant proliferation and activation of lung fibroblasts contribute to the initiation and progression of idiopathic pulmonary fibrosis (IPF). However, the mechanisms responsible for the proliferation and activation of fibroblasts are not fully understood. The objective of this study was to investigate the role of miR-101 in the proliferation and activation of lung fibroblasts. miR-101 expression was determined in lung tissues from patients with IPF and mice with bleomycin-induced pulmonary fibrosis. The regulation of miR-101 and cellular signaling was investigated in pulmonary fibroblasts The role of miR-101 in pulmonary fibrosis was studied using adenovirus-mediated gene transfer in mice. The expression of miR-101 was down-regulated in fibrotic lungs from patients with IPF and bleomycin-treated mice. The down-regulation of miR-101 occurred via the E26 transformation-specific (ETS) transcription factor. miR-101 suppressed the WNT5a-induced proliferation of lung fibroblasts by inhibiting NFATc2 signaling via targeting Frizzled receptor 4/6 and the TGF-β-induced activation of lung fibroblasts by inhibition of SMAD2/3 signaling via targeting the TGF-β receptor 1. Adenovirus-mediated miR-101 gene transfer in the mouse lung attenuated bleomycin-induced lung fibrosis and improved lung function. Our data suggest that miR-101 is an anti-fibrotic microRNA and a potential therapeutic target for pulmonary fibrosis.

Alveolar epithelial cell (AEC) trans-differentiation is a process where type II alveolar epithelial cells (AEC II) trans-differentiate into type I alveolar epithelial cells (AEC I) during lung recovery after various injuries, in which AEC I are damaged. This process is critical for lung tissue repair. MicroRNAs are a group of small RNAs that regulate gene expression at the post-transcriptional level. They have the potential to regulate almost every aspect of cell physiology. However, whether AEC trans-differentiation is regulated by microRNAs is completely unknown. In this study, we found that miR-375 was downregulated during AEC trans-differentiation. The overexpression of miR-375 with an adenoviral vector inhibited alveolar epithelial trans-differentiation as indicated by an increase in the AEC II marker, surfactant protein C, and decreases in the AEC I markers, T1α and advanced glycosylation end product-specific receptor. miR-375 also inhibited the Wnt/β-catenin pathway. The constitutively activation of Wnt/β-catenin signaling with a stabilized form of β-catenin blocked the miR-375 effects. Frizzled 8 was identified as a target of miR-375. In summary, our results demonstrate that miR-375 regulates AEC trans-differentiation through the Wnt/β-catenin pathway. This discovery may provide new targets for therapeutic intervention to benefit lung recovery from injuries.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and typically fatal lung disease with a very low survival rate. Excess accumulation of fibroblasts, myofibroblasts and extracellular matrix creates hypoxic conditions within the lungs, causing asphyxiation. Hypoxia is, therefore, one of the prominent features of IPF. However, there have been few studies concerning the effects of hypoxia on pulmonary fibroblasts. In this study, we investigated the molecular mechanisms of hypoxia-induced lung fibroblast proliferation. Hypoxia increased the proliferation of normal human pulmonary fibroblasts and IPF fibroblasts after exposure for 3–6 days. Cell cycle analysis demonstrated that hypoxia promoted the G1/S phase transition. Hypoxia downregulated cyclin D1 and A2 levels, while it upregulated cyclin E1 protein levels. However, hypoxia had no effect on the protein expression levels of cyclin-dependent kinase 2, 4, and 6. Chemical inhibition of hypoxia-inducible factor (HIF)-2 reduced hypoxia-induced fibroblast proliferation. Moreover, silencing of Nuclear Factor Activated T cell (NFAT) c2 attenuated the hypoxia-mediated fibroblasts proliferation. Hypoxia also induced the nuclear translocation of NFATc2, as determined by immunofluorescence staining. NFAT reporter assays showed that hypoxia-induced NFAT signaling activation is dependent on HIF-2, but not HIF-1. Furthermore, the inhibition or silencing of HIF-2, but not HIF-1, reduced the hypoxia-mediated NFATc2 nuclear translocation. Our studies suggest that hypoxia induces the proliferation of human pulmonary fibroblasts through NFAT signaling and HIF-2.