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The advancement of biomaterials with antimicrobial and wound healing properties continues to present challenges. Macrophages are recognized for their significant role in the repair of infection-related wounds. However, the interaction between biomaterials and macrophages remains complex and requires further investigation. In this research, we propose a new sequential immunomodulation method to enhance and expedite wound healing by leveraging the immune properties of bacteria-related wounds, utilizing a novel mixed hydrogel dressing. The hydrogel matrix is derived from porcine acellular dermal matrix (PADM) and is loaded with a new type of bioactive glass nanoparticles (MBG) doped with magnesium (Mg-MBG) and loaded with Curcumin (Cur). This hybrid hydrogel demonstrates controlled release of Cur, effectively eradicating bacterial infection in the early stage of wound infection, and the subsequent release of Mg ions (Mg2+) synergistically inhibits the activation of inflammation-related pathways (such as MAPK pathway, NF-κB pathway, TNF-α pathway, etc.), suppressing the inflammatory response caused by infection. Therefore, this innovative hydrogel can safely and effectively expedite wound healing during infection. Our design strategy explores novel immunomodulatory biomaterials, offering a fresh approach to tackle current clinical challenges associated with wound infection treatment. [ABSTRACT FROM AUTHOR]

Iron (Fe) is an essential trace element for plants, which is involved in photosynthesis and affected many important life activities of Vaccinium spp.. In order to explore the influence of Fe on the important life activities of blueberry (Vaccinium spp.), the blueberry 'Legacy' was used as the material, and 3 Fe environments were set: normal iron (Na-Fe-EDTA), insoluble iron only (Fe2O3) and iron deficiency (without any iron element). The relative chlorophyll content (SPAD value), chlorophyll content and chlorophyll fluorescence parameters of blueberry were analyzed. The results showed that in 2 stress environments of insoluble iron and iron deficiency, the growth indicators, photosynthetic pigment content and SPAD were significantly lower than those under normal iron environment (P< 0.05), while the number, growth amount, ground diameter, leaf area and leaf photosynthetic pigment content of basal branches of blueberry under insoluble iron environment were significantly lower than those in iron-deficient environment (P<0.05). The actual photosynthetic efficiency of leaf PS II under normal iron stress were higher than those under insoluble iron and iron deficiency, while the degree of photoinhibition were significantly lower than those under iron stress and iron deficiency. Leaves of seedlings were damaged and photosynthetic capacity of leaves was weakened in iron-insoluble and iron-deficient environments. The photosystem center conversion efficiency was more unstable in ironinsoluble environments than in iron-deficient environments, and blueberry leaves were the most photoinhibited. Leaf area, biomass per plant and growth of basal shoots were significantly correlated with chlorophyll fluorescence parameters (P<0.01), and photosynthetic pigment content of leaves was significantly positively correlated with SPAD value (P<0.01), but there was no significant correlation between photosynthetic pigment and SPAD and fluorescence parameters (P>0.01). In conclusion, insoluble iron, iron deficiency environment made blueberry growth inhibition and resulted in a decreased leaf chlorophyll content, leaf PS II stress environment reaction center absorption and conversion of light energy was abated, electron transfer and photosynthetic efficiency was lower, which provided reference for deep mining for blueberries in iron nutrient reasonable use way. [ABSTRACT FROM AUTHOR]

Pb-free piezoelectric ceramic materials (K0.48Na0.48Li0.04)(Nb0.92Ta0.08−xSbx)O3 (KNLNTS) were designed and prepared. The effects of varied Sb/Ta doping on the physical structure, surface morphology, and electrical characteristics of ceramics were also studied. The perovskite structure is present in all of the doped ceramic samples without any secondary phase (when x < 0.05). All of the doped ceramic samples have a Curie temperature (TC) above 300°C. At the same time, the orthorhombic–tetragonal phase transition temperature (TO–T) is pushed closer to ambient temperature. Doping with Sb/Ta/Li changed the electrical characteristics of the samples and increased their piezoelectric properties. At x = 0.03, the KNLNTS sample has the best piezoelectric properties: d33 = 215 pC/N, Pr = 26.08 μC/cm2, TC = 342.6°C. [ABSTRACT FROM AUTHOR]

Yes associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) are ubiquitous transcriptional co-activators that control organ development, homeostasis, and tissue regeneration. Current in vivo evidence suggests that YAP/TAZ regulates enamel knot formation during murine tooth development, and is indispensable for dental progenitor cell renewal to support constant incisor growth. Being a critical sensor for cellular mechano-transduction, YAP/TAZ lays at the center of the complex molecular network that integrates mechanical cues from the dental pulp chamber and surrounding periodontal tissue into biochemical signals, dictating in vitro cell proliferation, differentiation, stemness maintenance, and migration of dental stem cells. Moreover, YAP/TAZ-mediated cell-microenvironment interactions also display essential regulatory roles during biomaterial-guided dental tissue repair and engineering in some animal models. Here, we review recent advances in YAP/TAZ functions in tooth development, dental pulp, and periodontal physiology, as well as dental tissue regeneration. We also highlight several promising strategies that harness YAP/TAZ activation for promoting dental tissue regeneration. [ABSTRACT FROM AUTHOR]

Tooth development is a complex process that is tightly controlled by circadian rhythm. Melatonin (MT) is a major hormonal regulator of the circadian rhythm, and influences dentin formation and odontoblastic differentiation during tooth development; however, the underlying mechanism remains elusive. This study investigated how MT regulates odontoblastic differentiation, with a special focus on its regulation of mitochondrial dynamics. In rat dental papilla cells (DPCs), we found that MT promotes odontoblastic differentiation concurrently with enhanced mitochondrial fusion, while disruption of mitochondrial fusion by depleting optic atrophy 1 (OPA1) impairs MT‐mediated differentiation and mitochondrial respiratory functions. Through RNA sequencing, we discovered that MT significantly upregulated malic enzyme 2 (ME2), a mitochondrial NAD(P)+‐dependent enzyme, and identified ME2 as a critical MT downstream effector that orchestrates odontoblastic differentiation, mitochondrial fusion, and respiration functions. By detecting the spatiotemporal expression of ME2 in developing tooth germs, and using tooth germ reconstituted organoids, we also provided in vivo and ex vivo evidence that ME2 promotes dentin formation, indicating a possible involvement of ME2 in MT‐modulated tooth development. Collectively, our findings offer novel understandings regarding the molecular mechanism by which MT affects cell differentiation and organogenesis, meanwhile, the critical role of ME2 in MT‐regulated mitochondrial functions is also highlighted. [ABSTRACT FROM AUTHOR]

Background: The sympathetic nervous system (SNS) is suggested to be involved in some forms of pain, but the mechanisms of which are incompletely known. Moreover, there is a lack of information on the regulatory role of the SNS on macrophages in sensory ganglion, which plays an important role in pain development. The present study aims to investigate the effects of the SNS on orofacial inflammatory pain and examine, if any, how the SNS influences trigeminal ganglion (TG) macrophage responses. Methods: Sympathectomy was performed on male C57BL/6 mice before receiving a local injection of Complete Freund's adjuvant (CFA) to induce inflammatory pain. Effects of sympathectomy on orofacial pain were examined by Von Frey test and c-Fos expression. Polarization of TG macrophage was evaluated by immunohistochemistry and the level of norepinephrine (NE) in the TG were determined by liquid chromatography. Sympathetic signaling to TG macrophages were predicted based on single-cell analysis. Results: CFA injection induced a significant increase in mechanical allodynia, the number of c-Fos-positive neuron, and the level of NE in TG, which were largely reduced by sympathectomy. The number of M1 macrophages was markedly increased by CFA and was largely reduced by sympathectomy from 1 to 14 days post-injection. Single-cell RNA sequencing analysis and immunofluorescence staining showed that TG macrophages mainly express β 2 adrenergic receptors for NE. Cell–cell communication analysis predicted sympathetic signaling that may modulate macrophage phenotypes, including Colony-stimulating factor-1, Migration inhibitory factor, Pleiotrophin and Nicotinamide phosphoribosyl transferase. Conclusion: The SNS may involve in CFA-induced mechanical allodynia via modulating macrophage phenotypes in the TG. Targeting sympathetic activation might be useful in treating some painful conditions in the orofacial region. [ABSTRACT FROM AUTHOR]

Orofacial inflammation leads to transcriptional alterations in trigeminal ganglion (TG) neurons. However, diverse alterations and regulatory mechanisms following orofacial inflammatory pain in different types of TG neurons remain unclear. Here, orofacial inflammation was induced by injection of complete Freund's adjuvant (CFA) in mice. After 7 days, we performed single-cell RNA-sequencing on TG cells of mice from control and treatment groups. We identified primary sensory neurons, Schwann cells, satellite glial cells, oligodendrocyte-like cells, immune cells, fibroblasts, and endothelial cells in TG tissue. After principal component analysis and hierarchical clustering, we identified six TG neuronal subpopulations: peptidergic nociceptors (PEP1 and PEP2), non-peptidergic nociceptors (NP1 and NP2), C-fiber low-threshold mechanoreceptors (cLTMR) and myelinated neurons (Nefh -positive neurons, NF) based on annotated marker gene expression. We also performed differential gene expression analysis among TG neuronal subtypes, identifying several differential genes involved in the inflammatory response, neuronal excitability, neuroprotection, and metabolic processes. Notably, we identified several potential novel targets associated with pain modulation, including Arl6ip1 , Gsk3b , Scn7a , and Zbtb20 in PEP1, Rgs7bp in PEP2, and Bhlha9 in cLTMR. The established protein–protein interaction network identified some hub genes, implying their critical involvement in regulating orofacial inflammatory pain. Our study revealed the heterogeneity of TG neurons and their diverse neuronal transcriptomic responses to orofacial inflammation, providing a basis for the development of therapeutic strategies for orofacial inflammatory pain. [ABSTRACT FROM AUTHOR]

Apical periodontitis (AP) causes arrest of tooth root development, which is associated with impaired odontoblastic differentiation of stem cells from apical papilla (SCAPs), but the underlying mechanism remains unclear. Here, we investigated roles of extracellular vesicle (EV) in AP and odontoblastic differentiation of SCAPs, moreover, a novel nuclear factor I/C (NFIC)-encapsulated EV was developed to promote dentin regeneration. We detected a higher expression of EV marker CD63 in inflamed apical papilla, and found that EVs from LPS-stimulated dental pulp cells suppressed odontoblastic differentiation of SCAPs through downregulating NFIC. Furthermore, we successfully constructed the NFIC-encapsulated EV by overexpressing NFIC in HEK293FT cells, which could upregulate cellular NFIC level in SCAPs, promoting the proliferation and migration of SCAPs, as well as dentinogenesis both in vitro and in vivo. Collectively, based on pathological roles of EV in AP, our study provides a novel strategy for dentin regeneration by exploiting EV to deliver NFIC. [ABSTRACT FROM AUTHOR]

Autophagy is an evolutionarily conserved cellular process, in which damaged organelles and proteins are engulfed in autophagic vesicles and subsequently fuse with lysosomes for degradation. Autophagy is widely involved in different physiologic or pathologic processes in human. Accumulating evidence indicates that autophagy operates as a critical quality control mechanism to maintain pulp homeostasis and structural integrity of the dentin‐pulp complex. Autophagy is activated during stresses and is involved in the pathogenesis of pulpitis and periapical infection. Recent discoveries have also provided intriguing insights into the roles of autophagy in tooth development, pulp aging and stress adaptation. In this review, we provide an update on the multifaceted functions of autophagy in physiology and pathophysiology of tooth. We also discuss the therapeutic implications of autophagy modulation in diseases and the regeneration of dentin‐pulp complex. [ABSTRACT FROM AUTHOR]

The activation of opioid receptors by exogenous or endogenous opioids can produce significant analgesic effects in peripheral tissues. Numerous researchers have demonstrated the expression of peripheral opioid receptors (PORs) and endogenous opioid peptides (EOPs) in the orofacial region. Growing evidence has shown the involvement of PORs and immune cell-derived EOPs in the modulation of orofacial pain. In this review, we discuss the role of PORs and EOPs in orofacial pain and the possible cellular mechanisms involved. Furthermore, the potential development of therapeutic strategies for orofacial pain is also summarized. [ABSTRACT FROM AUTHOR]

Manipulating light polarization is of fundamental importance in the modern photonic applications such as spectroscopy, laser science, optical communication, quantum information processing, chemical and biological sensing. Polarization control of light is typically achieved by natural chiral or birefringent materials with macroscopic volume due to the weak light–matter interaction. Here, a folded eta‐shaped metamaterial that is capable of generating gigantic optical chirality and spectrally breaking the spin degeneracy of optical transmission at multiband is experimentally demonstrated. The intrinsic chiral configuration is achieved by folding the eta‐shaped metasurface along the vertical direction to break the mirror symmetries. A remarkable circular dichroism approaching unity is experimentally achieved, with the maximum transmittance exceeding 93%. This is the record high value demonstrated to date for single‐layer metasurfaces without diffraction in infrared region. The folded metamaterial provides a straightforward strategy for achieving intrinsic 3D chirality and has great potential for applications in photon‐spin selective devices and chiral biomolecule identification. [ABSTRACT FROM AUTHOR]