Background: Chronic rhinosinusitis (CRS) is an inflammatory condition classified into chronic rhinosinusitis with nasal polyps (CRSwNP) and chronic rhinosinusitis without nasal polyps (CRSsNP). Th cells manage inflammatory cells in CRS. Suppressor of Cytokine Signaling (SOCS) proteins regulate Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway in Th cells by polarizing toward Th1, Th2, and Th17 cells. This study evaluated the levels of SOCS1,3,5 in CRS patients to find associations with Th cells. Methods: In this cross-sectional study, 20 CRSwNP patients, 12 CRSsNP patients, and 12 controls participated. The infiltration of CD4+ T cells was determined using immunohistochemistry. The expression of specific transcription factors and SOCS proteins was assessed using real-time PCR. Cytokine levels were evaluated using ELISA. SOCS protein levels were investigated using western blot analysis. Results: The expression of SOCS3 increased in the CRSwNP group compared to CRSsNP and control groups (p <0.001). SOCS3 protein levels increased in the CRSwNP group compared to CRSsNP (p <0.05) and control (p <0.001) groups. Although there was a significant difference in SOCS5 expression between CRSsNP and control groups, SOCS5 protein levels were significantly different between CRSsNP and control (p <0.001) and CRSwNP (p <0.05) groups. Conclusions: Targeted therapies may be suggested for CRS by modulating SOCS3 and SOCS5 proteins that are responsible for polarization of Th cells toward Th2 or Th1 cells, respectively. JAK-STAT pathway targeting, which encompasses numerous cells, can be limited to SOCS proteins to more effectively orchestrate Th cell differentiation.

A complete framework of predicting the attributes of sea clutter under different operational conditions, specified by wind speed, wind direction, grazing angle, and polarization, is proposed for the first time. This framework is composed of empirical spectra to characterize sea-surface profiles under different wind speeds, the Monte Carlo method to generate realizations of sea-surface profiles, the physical-optics method to compute the normalized radar cross-sections (NRCSs) from individual sea-surface realizations, and regression of NRCS data (sea clutter) with an empirical probability density function (PDF) characterized by a few statistical parameters. JONSWAP and Hwang ocean-wave spectra are adopted to generate realizations of sea-surface profiles at low and high wind speeds, respectively. The probability density functions of NRCSs are regressed with K and Weibull distributions, each characterized by two parameters. The probability density functions in the outlier regions of weak and strong signals are regressed with a power-law distribution, each characterized by an index. The statistical parameters and power-law indices of the K and Weibull distributions are derived for the first time under different operational conditions. The study reveals succinct information of sea clutter that can be used to improve the radar performance in a wide variety of complicated ocean environments. The proposed framework can be used as a reference or guidelines for designing future measurement tasks to enhance the existing empirical models on ocean-wave spectra, normalized radar cross-sections, and so on.

Copolymers based on vinylidene fluoride are potential materials for ferroelectric memory elements. The trend in studies showing that a decrease in the degree of crystallinity can lead to an unexpected increase in the electric breakdown field is noted. An analysis of the literature data reveals that in fluorine-containing ferroelectric polymers, when using a bipolar triangular field, the hysteresis loop has an unclosed shape, with each subsequent loop being accompanied by a decrease in the dielectric response. In this work, the effect of the structure of self-polarized films of copolymers of vinylidene fluoride with tetrafluoroethylene and hexafluoropropylene on breakdown processes was studied. The structure of the polymer films was monitored using infrared spectroscopy (IR) and X-ray diffraction. Kelvin probe force microscopy (KPFM) was applied to characterize the local electrical properties of the polymers. For the films of the first copolymer, which crystallize in the polar β-phase, asymmetry in the dielectric response was observed at fields greater than the coercive field. For the films of the copolymers of vinylidene fluoride with hexafluoropropylene, which crystallize predominantly in the nonpolar α-phase, polarization switching processes have also been observed, but at lower electric fields. The noted phenomena will help to identify the influence of the structure of ferroelectric polymers on their electrical properties.

Lupus nephritis (LN) is a severe and common manifestation of systemic lupus erythematosus (SLE) that is frequently identified with a poor prognosis. Macrophages play an important role in its pathogenesis. Different macrophage subtypes have different effects on lupus-affected kidneys. Based on their origin, macrophages can be divided into monocyte-derived macrophages (MoMacs) and tissue-resident macrophages (TrMacs). During nephritis, TrMacs develop a hybrid pro-inflammatory and anti-inflammatory functional phenotype, as they do not secrete arginase or nitric oxide (NO) when stimulated by cytokines. The infiltration of these mixed-phenotype macrophages is related to the continuous damage caused by immune complexes and exposure to circulating inflammatory mediators, which is an indication of the failure to resolve inflammation. On the other hand, MoMacs differentiate into M1 or M2 cells under cytokine stimulation. M1 macrophages are pro-inflammatory and secrete pro-inflammatory cytokines, while the M2 main phenotype is essentially anti-inflammatory and promotes tissue repair. Conversely, MoMacs undergo differentiation into M1 or M2 cells in response to cytokine stimulation. M1 macrophages are considered pro-inflammatory cells and secrete pro-inflammatory mediators, whereas the M2 main phenotype is primarily anti-inflammatory and promotes tissue repair. Moreover, based on cytokine expression, M2 macrophages can be further divided into M2a, M2b, and M2c phenotypes. M2a and M2c have anti-inflammatory effects and participate in tissue repair, while M2b cells have immunoregulatory and pro-inflammatory properties. Further, memory macrophages also have a role in the advancement of LN. Studies have demonstrated that the polarization of macrophages is controlled by multiple metabolic pathways, such as glycolysis, the pentose phosphate pathway, fatty acid oxidation, sphingolipid metabolism, the tricarboxylic acid cycle, and arginine metabolism. The changes in these metabolic pathways can be regulated by substances such as fish oil, polyenylphosphatidylcholine, taurine, fumaric acid, metformin, and salbutamol, which inhibit M1 polarization of macrophages and promote M2 polarization, thereby alleviating LN.

BACKGROUND: An event of increasing interest during host-pathogen interactions is the polarization of patrolling/naive monocytes (MOs) into macrophage subsets (MФs). Therapeutic strategies aimed at modulating this event are under investigation.
METHODS: This review focuses on the mechanisms of induction/development and profile of MФs polarized toward classically proinflammatory (M1) or alternatively anti-inflammatory (M2) phenotypes in response to bacteria, fungi, parasites, and viruses.
CONCLUSIONS: It highlights nuclear, cytoplasmic, and cell surface receptors (pattern recognition receptors/PPRs), microenvironmental mediators, and immune signaling. MФs polarize into phenotypes: M1 MФs, activated by IFN-γ, pathogen-associated molecular patterns (PAMPs, e.g. lipopolysaccharide) and membrane-bound PPRs ligands (TLRs/CLRs ligands); or M2 MФs, induced by interleukins (ILs-4, -10 and -13), antigen-antibody complexes, and helminth PAMPs. Polarization toward M1 and M2 profiles evolve in a pathogen-specific manner, with or without canonicity, and can vary widely. Ultimately, this can result in varying degrees of host protection or more severe disease outcome. On the one hand, the host is driving effective MФs polarization (M1 or M2); but on the other hand, microorganisms may skew the polarization through virulence factors to increase pathogenicity. Cellular/genomic reprogramming also ensures plasticity of M1/M2 phenotypes. Because modulation of polarization can occur at multiple points, new insights and emerging perspectives may have clinical implications during the inflammation-to-resolution transition; translated into practical applications as for therapeutic/vaccine design target to boost microbicidal response (M1, e.g. triggering oxidative burst) with specifics PAMPs/IFN-γ or promote tissue repair (M2, increasing arginase activity) via immunotherapy.
Monocytes are white blood cells (leukocytes) that help fight off various types of aggressive agents, including microorganisms (bacteria, fungi, viruses, and parasites), and help maintain the healthy balance of the human body. These cells differentiate into specific macrophages in tissues such as the lungs, heart, liver, skin, and brain. The present review focuses on the peculiar cellular properties that macrophages can acquire during the human immune response to infectious diseases. In this regard, it is discussed that macrophages are didactically divided into M1 and M2 subtypes. The first subtype (M1) is responsible for fighting pathogens and causing inflammation. The second subtype (M2) is mainly responsible for healing and repairing damaged tissue. Current knowledge shows that although both subtypes are involved in the same immune response aimed at protecting the human body, these M1 and M2 profiles have different characteristics that have implications for therapeutic measures such as developing specific drugs or vaccines to balance the immune response against a given pathogen and promote a complete cure of the disease. Alongside the therapeutic impacts, this review also looks at the characteristics that allow aggressive microorganisms to counteract the immune response developed by these M1 and M2 cell profiles. It highlights how exactly there can be greater protection or detriment to the human host against a given microorganism when there is a predilection to develop a more abundant immune response from one of the two profiles (M1 or M2).

BACKGROUND: Periodontitis is a common oral disease with high prevalence worldwide. Neural epidermal growth factor-like 1 protein (Nell-1) has recently been reported to have anti-inflammation effects and may be a drug candidate for osteoarthritis. However, its immunotherapeutic effects in periodontitis remain unknown. Therefore, this study aimed to investigate the effects of Nell-1 on periodontitis in terms of macrophage polarization and analyze its possible underlying mechanism.
METHODS: A rat ligation-induced experimental periodontitis model was established and locally injected with Nell-1 (n = 6/group). Periodontal tissue destruction and macrophage polarization in vivo were analyzed using micro-CT, histology analysis, and western blot. Enzyme-linked immunosorbent assay was used to evaluate serum inflammatory cytokines. Then, the RAW 264.7 macrophage cells were treated with lipopolysaccharide (LPS), Nell-1, and the c-Jun N-terminal kinases (JNK) inhibitor (SP600125). RT-PCR, western blot, and flow cytometry were performed to further analyze the effect of Nell-1 on macrophage polarization and the underlying mechanism in vitro.
RESULTS: Local treatment with Nell-1 significantly alleviated the destruction of alveolar bone and fibers in periodontitis, and upregulated the ratio of M2/M1 macrophages in periodontal tissues (P < 0.05). In vitro, Nell-1 at the concentrations of 200 and 500 ng/mL could significantly inhibit the expression of M1-related inflammatory factors in LPS-stimulated macrophages, and increase the expression of M2-related markers, regulating the macrophage phenotype switch into M2 (P < 0.05). The mRNA of JNK and relative protein level of phospho-JNK/JNK were also upregulated by Nell-1 (P < 0.05). Additionally, the JNK inhibitor (SP600125) could reverse the effect of Nell-1 on macrophage polarization (P < 0.05).
CONCLUSIONS: Nell-1 could modulate the ratio of M2/M1 macrophages possibly through the JNK/MAPK signaling pathway, subsequently attenuating the inflammation and destruction of periodontal tissues caused by periodontitis.

Small Cu clusters are excellent candidates for the electrocatalytic reduction of carbon dioxide (CO2RR), and their catalytic performance is expected to be significantly influenced by the interaction between the substrate and cluster. In this study, we systematically investigate the CO2RR for a Cu3 cluster anchored on Janus MoSX (X = Se, Te) substrates using density functional theory calculations. These substrates feature a broken vertical mirror symmetry, which generates spontaneous out-of-plane polarization and offers two distinct polar surfaces to support the Cu3 cluster. Our findings reveal that the CO2RR performance on the Cu3 cluster is strongly influenced by the polarization direction and strength of the MoSX (X = Se, Te) substrates. Notably, the Cu3 cluster supported on the S-terminated MoSTe surface (Cu3(S)@MoSTe) demonstrates the highest CO2RR activity, producing methane. These results underscore the pivotal role of substrate polarization in modulating the binding strength of reactants and reaction intermediates, thereby enhancing the CO2RR efficiency.

While artificial 3D nanostructures can generate precise and flexible coloration, their real-time color changes during 3D nanoprinting remain unexplored owing to the inherent challenges of in situ transient measurements and observations. In this study, a 3D-printing system which supports the operando observation/measurement of the color dynamics of subwavelength metallic nanoarchitectures fabricated in real time is developed and evaluated. During 3D printing, the dimensions and geometries of the 3D nanostructures grow over time, producing a large library of optical spectra associated with real-time color changes. Only a timer is needed to define the expected colors from a single 3D print run. Fin-like nanostructures are used to toggle colors based on the polarization effect and produce color gradients. Based on structural coloration, nanoarchitectures are designed and printed to animate desired color patterns. Moreover, the resulting color dynamics can also serve as an operando identifier for real-time structural information during 3D nanoprinting. A single print run enables the efficient creation of a comprehensive library of desired colorations owing to the flexibility in time-dependent controllability and 3D geometries at the subwavelength scale. 3D nanoprinted plasmonic structures exhibiting time-varying colorations (4D printing of colors) uniquely redefines the coloring stategy, offering considerable potential for numerous applications.

Neuroinflammation and microglia polarization play pivotal roles in brain injury induced by intracerebral hemorrhage (ICH). Despite the well-established involvement of CXC motif chemokine ligand 16 (CXCL16) in regulating inflammatory responses across various diseases, its specific functions in the context of neuroinflammation and microglial polarization following ICH remain elusive. In this study, we investigated the impact of CXCL16 on neuroinflammation and microglia polarization using both mouse and cell models. Our findings revealed elevated CXCL16 expression in mice following ICH and in BV2 cells after lipopolysaccharide (LPS) stimulation. Specific silencing of CXCL16 using siRNA led to a reduction in the expression of neuroinflammatory factors, including IL-1β and IL-6, as well as decreased expression of the M1 microglia marker iNOS. Simultaneously, it enhanced the expression of anti-inflammatory factors such as IL-10 and the M2 microglia marker Arg-1. These results were consistent across both mouse and cell models. Intriguingly, co-administration of the PI3K-specific agonist 740 Y-P with siRNA in LPS-stimulated cells reversed the effects of siRNA. In conclusion, silencing CXCL16 can positively alleviate neuroinflammation and M1 microglial polarization in BV2 inflammation models and ICH mice. Furthermore, in BV2 cells, this beneficial effect is mediated through the PI3K/Akt pathway. Inhibition of CXCL16 could be a novel approach for treating and diagnosing cerebral hemorrhage.

The pancreas is an organ with both exocrine and endocrine functions, comprising a highly organized and complex tissue microenvironment composed of diverse cellular and non-cellular components. The impairment of microenvironmental homeostasis, mediated by the dysregulation of cell-to-cell crosstalk, can lead to pancreatic diseases such as pancreatitis, diabetes, and pancreatic cancer. Macrophages, key immune effector cells, can dynamically modulate their polarization status between pro-inflammatory (M1) and anti-inflammatory (M2) modes, critically influencing the homeostasis of the pancreatic microenvironment and thus playing a pivotal role in the pathogenesis of the pancreatic disease. This review aims to summarize current findings and provide detailed mechanistic insights into how alterations mediated by macrophage polarization contribute to the pathogenesis of pancreatic disorders. By analyzing current research comprehensively, this article endeavors to deepen our mechanistic understanding of regulatory molecules that affect macrophage polarity and the intricate crosstalk that regulates pancreatic function within the microenvironment, thereby facilitating the development of innovative therapeutic strategies that target perturbations in the pancreatic microenvironment.