Endometriosis is a chronic estrogen-dependent disease characterized by the presence of endometrial glands and stroma outside their normal anatomical location. While laparoscopic removal of foci remains the gold standard therapy, it has limited efficacy and certain risks. However, cell therapy using pro-inflammatory M1 macrophages presents a promising and minimally invasive alternative for treating endometriosis. This approach showcases the potential for innovative and effective treatments for this condition. This study aims to explore the anti-endometriosis properties of M1 macrophages. A reproducible syngeneic mouse model of endometriosis was utilized, revealing that formed foci are primarily composed of macrophages with an anti-inflammatory M2 phenotype rather than M1 macrophages. To investigate further, chemically reprogrammed M1 macrophages were labeled with the membrane fluorescent tag PKH26 and administered to animals with endometriosis. Therapy resulted in a decrease in the number and size of foci, accompanied by a shift in the phenotypic composition of peritoneal macrophages. Specifically, the content of M2 macrophages decreased while that of M1 macrophages increased, resembling the composition of healthy animals. Our study conclusively demonstrates the anti-endometriosis properties of M1 macrophages, providing a strong foundation for future research in the cell therapy of endometriosis.

UNASSIGNED: Although spatial frequency domain imaging (SFDI) has been well characterized under diffuse optical conditions, tissue measurements made outside the diffuse regime can provide new diagnostic information. Before such measurements can become clinically relevant, however, the behavior of sub-diffuse SFDI and its effect on the accuracy of derived tissue parameters must be assessed.
UNASSIGNED: We aim to characterize the impact that both the assumed scattering phase function (SPF) and the polarization state of the illumination light source have on the accuracy of SFDI-derived optical properties when operating under diffuse or sub-diffuse conditions, respectively.
UNASSIGNED: Through the use of a set of well-characterized optical phantoms, SFDI accuracy was assessed at four wavelengths (395, 545, 625, and 850 nm) and two different spatial frequencies (0.3 and 1.0    mm - 1 ), which provided a broad range of diffuse and sub-diffuse conditions, using three different SPFs. To determine the effects of polarization, the SFDI accuracy was assessed using both unpolarized and cross-polarized illumination.
UNASSIGNED: It was found that the assumed SPF has a direct and significant impact on the accuracy of the SFDI-derived optical properties, with the best choice of SPF being dictated by the polarization state. As unpolarized SFDI retains the sub-diffuse portion of the signal, optical properties were found to be more accurate when using the full SPF that includes forward and backscattering components. By contrast, cross-polarized SFDI yielded accurate optical properties when using a forward-scattering SPF, matching the behavior of cross-polarization to attenuate the immediate backscattering of sub-diffuse reflectance. Using the correct pairings of SPF and polarization enabled using a reflectance standard, instead of a more subjective phantom, as the reference measurement.
UNASSIGNED: These results provide the foundation for a more thorough understanding of SFDI and enable new applications of this technology in which sub-diffuse conditions dominate (e.g., μ a ≮ μ s \' ) or high spatial frequencies are required.

The study aims to investigate the effects and potential mechanisms of lncRNA-MM2P on retinal neovascularization in a mouse model of oxygen-induced retinopathy (OIR). The OIR model was established in C57BL/6J mice. RAW264.7 cell line and bone marrow-derived macrophages (BMDMs) from mice were used for in vitro studies. RT-qPCR was used to analyze the expressions of lncRNA and mRNAs. The protein expression levels were determined by western blotting. The size of avascular areas and neovascular tufts were assessed based on isolectin B4 immunofluorescence staining images. The human retinal endothelial cells (HRECs) were used to evaluate the proliferation, migration, and tube formation of endothelial cells. The expression of lncRNA-MM2P was significantly upregulated from P17 to P25 in OIR retinas. Knockdown of lncRNA-MM2P levels in vivo led to a significant reduction in the neovascular tufts and avascular areas in the retinas of OIR mice. Knockdown of lncRNA-MM2P levels in vitro suppressed the expression of M2 markers in macrophages. Moreover, we found a significant inhibition of avascular areas and neovascular tufts in OIR mice injected intravitreally with M2 macrophages treated by shRNA-MM2P. The cellular functions of proliferation, migration, and tube formation were significantly attenuated in HRECs cultured with a supernatant of shRNA-MM2P-treated M2 macrophages. Our results indicate that lncRNA-MM2P regulates retinal neovascularization by inducing M2 polarization of macrophages in OIR mice. Therefore, lncRNA-MM2P may be a potential molecular target for immunoregulation of retinal neovascularization.

Optical properties determine how light interacts with biological tissues. The current methods for measuring these optical properties are influenced by both deep and superficial skin layers. Polarization-based methods have been proposed in order to determine the influence of deep layer scattering. Polarized light allows for the separation of ballistic photons from diffuse ones, enhancing image contrast and resolution while providing additional tissue information. The Q-sensing technique captures co-polarized I ∥ $$ \\left({I}_{\\parallel}\\right) $$ and cross-polarized I ⊥ $$ \\left({I}_{\\perp}\\right) $$ signals, making it possible to isolate the superficial scattering. However, the random structure of tissues leads to rapid depolarization of the polarized light. Detecting where the light becomes depolarized aids in sensing abnormalities within the tissues. Hence, this research focuses on identifying where depolarization occurs within the tissue. Tissue-mimicking phantoms, simulating the optical properties of biological tissues, are created to measure depolarization at various thicknesses. Experimental findings are validated with a Monte Carlo simulation, modeling polarized light behavior through the polydisperse tissue (as the tissue scatterers are heterogeneous in size). Additionally, the research demonstrates how polarized light can extract the optical properties of the medium.

In this article, we have explored the use of Mueller polarimetry for the detection and enhancement of alterations in questioned documents. Erasures, obliterations (with liquid paper and by pasting an additional layer of paper), and insertions (made with several inks) were studied in both regular and glossy paper. Promising results were obtained, which depend on the type of paper and the relation between the color of the ink and that of the illuminating light source. Erasures are easier to detect in glossy paper than in regular paper. Obliterations with liquid paper produced successful results in both types of paper, while detection of obliterations made with an additional layer of paper led to higher contrast for regular paper. Regarding the insertions, the black ball-point ink could be differentiated from roller-ball and gel-pen ink, which is often difficult to achieve visually. The contrast observed between the two inks was higher for regular paper than for glossy paper. Although the results shown in this article are promising, a wider variety of papers and pen types must be tested to further develop the procedure. It has the advantage of being non-destructive and far more economic than other methods. In some cases, the results can be complementary to those obtained by other methods (e.g., fluorescence with UV excitation and illumination with transmitted and oblique light), while in other cases the method offers unique advantages.

There is an association between noise exposure and cognitive impairment, and noise may have a more severe impact on patients with Alzheimer\'s disease (AD) and mild cognitive impairment; however, the mechanisms need further investigation. This study used the classic AD animal model APP/PS1 mice to simulate the AD population, and C57BL/6J mice to simulate the normal population. We compared their cognitive abilities after noise exposure, analyzed changes in Cluster of Differentiation (CD) between the two types of mice using transcriptomics, identified the differential CD molecule: CD36 in APP/PS1 after noise exposure, and used its pharmacological inhibitor to intervene to explore the mechanism by which CD36 affects APP/PS1 cognitive abilities. Our study shows that noise exposure has a more severe impact on the cognitive abilities of APP/PS1 mice, and that the expression trends of differentiation cluster molecules differ significantly between C57BL/6J and APP/PS1 mice. Transcriptomic analysis showed that the expression of CD36 in the hippocampus of APP/PS1 mice increased by 2.45-fold after noise exposure (p < 0.001). Meanwhile, Western Blot results from the hippocampus and entorhinal cortex indicated that CD36 protein levels increased by approximately 1.5-fold (p < 0.001) and 1.3-fold (p < 0.05) respectively, after noise exposure in APP/PS1 mice. The changes in CD36 expression elevated oxidative stress levels in the hippocampus and entorhinal cortex, leading to a decrease in PI3K/AKT phosphorylation, which in turn increased M1-type microglia and A1-type astrocytes while reducing the numbers of M2-type microglia and A2-type astrocytes. This increased neuroinflammation in the hippocampus and entorhinal cortex, causing synaptic and neuronal damage in APP/PS1 mice, ultimately exacerbating cognitive impairment. These findings may provide new insights into the relationship between noise exposure and cognitive impairment, especially given the different expression trends of CD molecules in the two types of mice, which warrants further research.

Konjac glucomannan (KGM) molecular chains contain a small amount of acetyl groups and a large number of hydroxyl groups, thereby exhibiting exceptional water retention and gel-forming properties. To meet diverse requirements, KGM undergoes modification processes such as oxidation, acetylation, grafting, and cationization, which reduce its viscosity, enhance its mechanical strength, and improve its water solubility. Researchers have found that KGM and its derivatives can regulate the polarization of macrophages, inducing their transformation into classically activated M1-type macrophages or alternatively activated M2-type macrophages, and even facilitating the interconversion between M1 and M2 phenotypes. Concurrently, the modulation of macrophage polarization states holds significant importance for chronic wound healing, inflammatory bowel disease (IBD), antitumor therapy, tissue engineering scaffolds, oral vaccines, pulmonary delivery, and probiotics. Therefore, KGM has the advantages of both immunomodulatory effects (biological activity) and gel-forming properties (physicochemical properties), giving it significant advantages in a variety of biomedical engineering applications.

Adult mammalian lungs exhibit a fractal pattern, as each successive generation of airways is a fraction of the size of the parental branch. Achieving this structure likely requires precise control of airway length and diameter, as the embryonic airways initially lack the fractal scaling observed in the adult. In monolayers and tubes, directional growth can be regulated by the planar cell polarity (PCP) complex. Here, we characterized the roles of PCP complex components in airway initiation, elongation and widening during branching morphogenesis of the lung. Using tissue-specific knockout mice, we surprisingly found that branching morphogenesis proceeds independently of PCP complex function in the lung epithelium. Instead, we found a previously unreported Celsr1-independent role for the PCP complex components Vangl1 and Vangl2 in the pulmonary mesenchyme, where they are required for branch initiation, elongation and widening. Our data thus reveal an explicit function for Vangl1 and Vangl2 that is independent of the core PCP complex, suggesting a functional diversification of PCP complex components in vertebrate development. These data also reveal an essential role for the embryonic mesenchyme in generating the fractal structure of airways in the mature lung.

The physical properties of a biomaterial play a vital role in modulating macrophage polarization. However, discerning the specific effects of individual parameters can be intricate due to their interdependencies, limiting the mechanism underlying a specific parameter on the polarization of macrophages. Here, we engineered silk fibroin (SF) films with tunable surface roughness while maintaining similar physical properties by combining casting and salting out techniques. We demonstrate that increased surface roughness in SF films promotes M2-like macrophage polarization, characterized by enhanced secretion of anti-inflammatory cytokines. Transcriptomic analysis unveils the modulation of genes associated with extracellular matrix-cell interactions, highlighting the role of surface topography in regulating cellular processes. Mechanistically, we show that surface roughness induces macrophage membrane curvature, facilitating integrin αv endocytosis and thereby inhibiting the integrin-NF-kB signaling pathway. In vivo implantation assays corroborate that rough SF films substantially mitigate early inflammatory responses. This work establishes a direct link between surface roughness and intracellular signaling in macrophages, adding to our understanding of the biomaterial surface effect at the material-cell interface and bringing insights into material design.

BACKGROUND: Opioid activation of the microglia or macrophage Toll-like receptor 4 (TLR4) and associated inflammatory cytokine release are implicated in opioid-induced hyperalgesia and tolerance. The cyclic GMP-AMP synthase/stimulator of interferon genes (cGAS-STING) signaling pathway, activated by double-stranded DNA including mitochondrial DNA (mtDNA), has emerged as another key mediator of inflammatory responses. This study tested the hypothesis that morphine induces immune inflammatory responses in microglia and macrophages involving TLR4 and cGAS-STING pathway.
METHODS: BV2 microglia and Raw 264.7 (Raw) macrophage cells were exposed to morphine with and without a STING inhibitor (C176) for 6 h or TLR 4 inhibitor (TAK242) for 24 h. Western blotting and RT-qPCR analyses assessed TLR4, cGAS, STING, nuclear factor-kappa B (NF-κB), and pro-inflammatory cytokine expression. Morphine-induced mitochondria dysfunction was quantified by reactive oxygen species (ROS) release using MitoSOX, mtDNA release by immunofluorescence, and RT-qPCR. Polarization of BV2 and Raw cells was assessed by inducible nitric oxide (iNOS) and CD86 expression. The role of mtDNA on morphine-related inflammation was investigated by mtDNA depletion of the cells with ethidium bromide (EtBr) or cell transfection of mtDNA extracted from morphine-treated cells.
RESULTS: Morphine significantly increased the expression of TLR4, cGAS, STING, p65 NF-κB, and cytokines (IL-6 and TNF-α) in BV2 and Raw cells. Morphine-induced mitochondrial dysfunction by increased ROS and mtDNA release; the increased iNOS and CD86 evidenced inflammatory M1-like phenotype polarization. TLR4 and STING inhibitors reduced morphine-induced cytokine release in both cell types. The transfection of mtDNA activated inflammatory signaling proteins, cytokine release, and polarization. Conversely, mtDNA depletion led to the reversal of these effects.
CONCLUSIONS: Morphine activates the cGAS-STING pathway in macrophage cell types. Inhibition of the STING pathway can be an additional method to overcome immune cell inflammation-related morphine tolerance and opioid-induced hyperalgesia.