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Strongly confined electromagnetic (EM) fields generated by tightly focused light beams are applied widely in nano‐optics due to their vectorial characteristics. The inclusion of the longitudinal polarized component plays a crucial role in both the physical characteristics and practical uses of tightly focused vector beams. The acquisition of the distributions of the three orthogonal polarized components of these fields is advantageous for the comprehensive examination of their captivating physical phenomena and possible applications. However, this continues to pose a noteworthy obstacle, especially in the case of the fields that are generated by high numerical aperture objectives. A novel approach is proposed to quantifying the three mutually perpendicular polarizations simultaneously in the focal plane. The method utilizes a dual‐mode waveguide probe that is composed of a dielectric nanoparticle and a metal‐dielectric waveguide. This design allows for the simultaneous support of both transverse electric (TE) and transverse magnetic (TM) modes. Consequently, it enables the polarization recognition of scattering light in k‐space. Importantly, this method effectively eliminates any interference originating from the background light. The work involves an analysis of the theoretical notion of the probe and followed by experimental investigations. This approach holds promise for augmenting optical nanoscopy methodologies and their associated applications. [ABSTRACT FROM AUTHOR]

The two-dimensional (2D) bulk photovoltaic effect (BPVE) is a cornerstone for future highly efficient 2D solar cells and optoelectronics. The ferromagnetic semiconductor 2H-FeCl2 is shown to realize a new type of BPVE in which spatial inversion (P), time reversal (T), and space–time reversal (PT) symmetries are broken (PT-broken). Using density functional theory and perturbation theory, we show that 2H-FeCl2 exhibits giant photocurrents, photo-spin-currents, and photo-orbital-currents under illumination by linearly polarized light. The injection-like and shift-like photocurrents coexist and propagate in different directions. The material also demonstrates substantial photoconductance, photo-spin-conductance, and photo-orbital-conductance, with magnitudes up to 4650 (nm·µA/V2), 4620 [nm·µA/V2ħ/(2e)], and 6450 (nm·µA/V2ħ/e), respectively. Furthermore, the injection-currents, shift-spin-currents, and shift-orbital-currents can be readily switched via rotating the magnetizations of 2H-FeCl2. These results demonstrate the superior performance and intriguing control of a new type of BPVE in 2H-FeCl2. [ABSTRACT FROM AUTHOR]

Aims: Mesenchymal stem cells (MSCs) present in the heart cannot differentiate into cardiomyocytes, but may play a role in pathological conditions. Therefore, the aim of this study was to scrutinise the role and mechanism of MSC differentiation in vivo during heart failure. Methods and Results: We performed single-cell RNA sequencing of total non-cardiomyocytes from murine and adult human hearts. By analysing the transcriptomes of single cells, we illustrated the dynamics of the cell landscape during the progression of heart hypertrophy, including those of stem cell antigen-1 (Sca1)+ stem/progenitor cells and fibroblasts. By combining genetic lineage tracing and bone marrow transplantation models, we demonstrated that non-bone marrow-derived Sca1+ cells give rise to fibroblasts. Interestingly, partial depletion of Sca1+ cells alleviated the severity of myocardial fibrosis and led to a significant improvement in cardiac function in Sca1-CreERT2;Rosa26-eGFP-DTA mice. Similar non-cardiomyocyte cell composition and heterogeneity were observed in human patients with heart failure. Mechanistically, our study revealed that Sca1+ cells can transform into fibroblasts and affect the severity of fibrosis through the Wnt4-Pdgfra pathway. Conclusions: Our study describes the cellular landscape of hypertrophic hearts and reveals that fibroblasts derived from Sca1+ cells with a non-bone marrow source largely account for cardiac fibrosis. These findings provide novel insights into the pathogenesis of cardiac fibrosis and have potential therapeutic implications for heart failure. Non-bone marrow-derived Sca1+ cells differentiate into fibroblasts involved in cardiac fibrosis via Wnt4-PDGFRα pathway. [ABSTRACT FROM AUTHOR]

Background: CD34+ cells have been used to treat the patients with heart failure, but the outcome is variable. It is of great significance to scrutinize the fate and the mechanism of CD34+ cell differentiation in vivo during heart failure and explore its intervention strategy. Methods: We performed single-cell RNA sequencing (scRNA-seq) of the total non-cardiomyocytes and enriched Cd34-tdTomato+ lineage cells in the murine (male Cd34-CreERT2; Rosa26-tdTomato mice) pressure overload model (transverse aortic constriction, TAC), and total non-cardiomyocytes from human adult hearts. Then, in order to determine the origin of CD34+ cell that plays a role in myocardial fibrosis, bone marrow transplantation model was performed. Furthermore, to further clarify the role of CD34 + cells in myocardial remodeling in response to TAC injury, we generated Cd34-CreERT2; Rosa26-eGFP-DTA (Cre/DTA) mice. Results: By analyzing the transcriptomes of 59,505 single cells from the mouse heart and 22,537 single cells from the human heart, we illustrated the dynamics of cell landscape during the progression of heart hypertrophy, including CD34+ cells, fibroblasts, endothelial and immune cells. By combining genetic lineage tracing and bone marrow transplantation models, we demonstrated that non-bone-marrow-derived CD34+ cells give rise to fibroblasts and endothelial cells, while bone-marrow-derived CD34+ cell turned into immune cells only in response to pressure overload. Interestingly, partial depletion of CD34+ cells alleviated the severity of myocardial fibrosis with a significant improvement of cardiac function in Cd34-CreERT2; Rosa26-eGFP-DTA model. Similar changes of non-cardiomyocyte composition and cellular heterogeneity of heart failure were also observed in human patient with heart failure. Furthermore, immunostaining showed a double labeling of CD34 and fibroblast markers in human heart tissue. Mechanistically, our single-cell pseudotime analysis of scRNA-seq data and in vitro cell culture study revealed that Wnt-β-catenin and TGFβ1/Smad pathways are critical in regulating CD34+ cell differentiation toward fibroblasts. Conclusions: Our study provides a cellular landscape of CD34+ cell-derived cells in the hypertrophy heart of human and animal models, indicating that non-bone-marrow-derived CD34+ cells differentiating into fibroblasts largely account for cardiac fibrosis. These findings may provide novel insights for the pathogenesis of cardiac fibrosis and have further potential therapeutic implications for the heart failure. [ABSTRACT FROM AUTHOR]

Hyperbolic metamaterials can support extremely high‐k wavevectors, also known as volume plasmon polaritons, with highly directional propagation and light confinement to deep‐subwavelength scales. The number of high‐k modes has an inverse relationship with the overall thickness of hyperbolic metamaterials. Here, the optical spin textures from high‐k mode polaritons on the surface of silica–silver multilayer hyperbolic metamaterials are studied. The results demonstrate that with an increase in the overall thickness, the spin texture changes from a twisted structure to a Néel‐type photonic skyrmion, due to the decrease in the number of high‐k modes. Moreover, the size of a single photonic skyrmion is less than 1/2 of the light wavelength, and the full width at half maximum of the spin angular momentum is less than 1/9 of the light wavelength. This work is expected to facilitate new applications of hyperbolic metamaterials, such as spin‐dependent excitation and detection devices at the deep‐subwavelength level. [ABSTRACT FROM AUTHOR]

The ambiguous results of multiple CD34+ cell-based therapeutic trials for patients with heart disease have halted the large-scale application of stem/progenitor cell treatment. This study aimed to delineate the biological functions of heterogenous CD34+ cell populations and investigate the net effect of CD34+ cell intervention on cardiac remodeling. We confirmed, by combining single-cell RNA sequencing on human and mouse ischemic hearts and an inducible Cd34 lineage-tracing mouse model, that Cd34+ cells mainly contributed to the commitment of mesenchymal cells, endothelial cells (ECs), and monocytes/macrophages during heart remodeling with distinct pathological functions. The Cd34+-lineage-activated mesenchymal cells were responsible for cardiac fibrosis, while CD34+Sca-1high was an active precursor and intercellular player that facilitated Cd34+-lineage angiogenic EC-induced postinjury vessel development. We found through bone marrow transplantation that bone marrow-derived CD34+ cells only accounted for inflammatory response. We confirmed using a Cd34-CreERT2; R26-DTA mouse model that the depletion of Cd34+ cells could alleviate the severity of ventricular fibrosis after ischemia/reperfusion (I/R) injury with improved cardiac function. This study provided a transcriptional and cellular landscape of CD34+ cells in normal and ischemic hearts and illustrated that the heterogeneous population of Cd34+ cell-derived cells served as crucial contributors to cardiac remodeling and function after the I/R injury, with their capacity to generate diverse cellular lineages. [ABSTRACT FROM AUTHOR]

Mycoplasma hyopneumoniae is considered the major causative agent of porcine respiratory disease complex, occurs worldwide and causes major economic losses to the pig industry. To gain more insights into the pathogenesis of this organism, the high throughput cDNA microarray assays were employed to evaluate host responses of porcine alveolar macrophages to M. hyopneumoniae infection. A total of 1033 and 1235 differentially expressed genes were identified in porcine alveolar macrophages in responses to exposure to M. hyopneumoniae at 6 and 15 hours post infection, respectively. The differentially expressed genes were involved in many vital functional classes, including inflammatory response, immune response, apoptosis, cell adhesion, defense response, signal transduction, protein folding, protein ubiquitination and so on. The pathway analysis demonstrated that the most significant pathways were the chemokine signaling pathway, Toll-like receptor signaling pathway, RIG-I-like receptor signaling pathway, nucleotide-binding oligomerization domains (Nod)-like receptor signaling pathway and apoptosis signaling pathway. The reliability of the data obtained from the microarray was verified by performing quantitative real-time PCR. The expression kinetics of chemokines was further analyzed. The present study is the first to document the response of porcine alveolar macrophages to M. hyopneumoniae infection. The data further developed our understanding of the molecular pathogenesis of M. hyopneumoniae.

Rationale: CD34+ cells are believed being progenitors that may be used to treat cardiovascular disease. However, the exact identity and the role of CD34+ cells in physiological and pathological conditions remain unclear. Methods: We performed single-cell RNA sequencing analysis to provide a cell atlas of normal tissue/organ and pathological conditions. Furthermore, a genetic lineage tracing mouse model was used to investigate the role of CD34+ cells in angiogenesis and organ fibrosis. Results: Single-cell RNA sequencing analysis revealed a heterogeneous population of CD34+ cells in both physiological and pathological conditions. Using a genetic lineage tracing mouse model, we showed that CD34+ cells not only acquired endothelial cell fate involved in angiogenesis, but also, CD34+ cells expressing Pi16 may transform into myofibroblast and thus participate in organ fibrosis. Conclusion: A heterogeneous CD34+ cells serve as a contributor not only to endothelial regeneration but also a wound healing response that may provide therapeutic insights into fibrosis. [ABSTRACT FROM AUTHOR]