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A facile, simple and low-cost approach for synthesizing highly fluorescent carbon quantum dots (CQDs) from thermal treatment of sustainable hair has been developed. The resultant CQDs exhibited strong blue emission with a quantum yield of 10.75%, excellent photostability and high stability in high salt conditions. As the fluorescence of CQDs can be efficiently quenched by Hg 2+ , the CQDs can be constructed as a nanosensor for Hg 2+ with good sensitivity and selectivity. And as low as 10 nM Hg 2+ can be successfully detected.

Ischemic stroke is common in the elderly, and it is one of the main causes of long-term disability worldwide. After ischemic stroke, spontaneous recovery and functional reconstruction take place. These processes are possible thanks to neuroplasticity, which involves neurogenesis, synaptogenesis, and angiogenesis. However, the repair of ischemic damage is not incomplete, and neurological deficits develop eventually. The WHO recommends acupuncture as an alternative and complementary method for the treatment of stroke. Moreover, clinical and experimental evidence has documented the potential of acupuncture to ameliorate ischemic stroke-induced neurological deficits, particularly sequelaes such as dyskinesia, spasticity, cognitive impairment, and dysphagia. These effects is related to the ability of acupuncture to promote spontaneous neuroplasticity after ischemic stroke. Specifically, acupuncture can stimulate neurogenesis, activate axon regeneration and sprouting, and improve the structure and function of synapses. These processes modify the neural network and function of the damaged brain area, producing the improvement of various skills and adaptability. Astrocytes and microglia may be involved in the regulation of acupuncture on neuroplasticity, such as the production and release of a variety of neurotrophic factors, including brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), neurotrophin-3 (NT-3), etc. Moreover, the presented evidence confirms that the functional reconstruction of the whole brain after ischemia plays an important role in the process of acupuncture regulating neuroplasticity. Therefore, neuroplasticity is expected to become a new target for acupuncture in the treatment of neurological deficits after ischemic stroke, and it is of great clinical value to conduct in-depth research and excavation on it.

Chronic low back pain (CLBP), lasting >3 months, is the end result of multiple pathogenic factors. Unfortunately, little is known about CLBP pathogenesis, which limits its advancements in clinical therapy and disease management. This paper summarizes the known pathological axes of CLBP, involving both peripheral and central systems. In particular, this paper details injurious nerve stimulation, inflammation-induced peripheral pathway, and central sensitization. Lumbar components, such as intervertebral disc (IVD), facet joints, muscles, fascia, ligaments, and joint capsules, contain pain receptors called nociceptors. Degeneration of the aforementioned lumbar components activates inflammatory pathways, which can directly damage nerves, lower nociceptor threshold to fire action potentials (AP), and cause pain. Additionally, damaged lumbar IVDs and endplates can also lead to the pathologic invasion of nerve growth and innervation, followed by the compression of herniated IVDs on nerve roots, thereby causing traumatic neuropathic pain. The central mechanism of CLBP involves alteration of the sensory processing of the brain and malfunction of the descending pain modulatory system, which facilitates pain amplification in the center nervous system (CNS). Lastly, abnormalities in the brain biochemical metabolism, activation of glial cells, and subsequent inflammation also play important roles in CLBP development. Taken together, inflammation plays an important role in both peripheral and central sensitization of CLBP. Due to the heterogeneity of CLBP, its pathological mechanism remains complex and difficult to understand. Therefore, it is a worthy field for future research into the subcomponents of CLBP pathogenesis, in order to distinguish the specific form of the disease, identify its origins, and develop corresponding highly effective comprehensive therapy against CLBP. Keywords: chronic low back pain, inflammation, degeneration, nerve innervation, central sensitization

Inflammatory pain is caused by peripheral tissue injury and inflammation. Inflammation leads to peripheral sensitization, which may further cause central sensitization, resulting in chronic pain and progressive functional disability. Neuroimmune crosstalk plays an essential role in the development and maintenance of inflammatory pain. Studies in recent years have shown that acupuncture can exert anti-inflammatory and analgesic effects by regulating peripheral (i.e., involving local acupoints and inflamed regions) and central neuroimmune interactions. At the local acupoints, acupuncture can activate the TRPV1 and TRPV2 channels of mast cells, thereby promoting degranulation and the release of histamine, adenosine, and other immune mediators, which interact with receptors on nerve endings and initiate neuroimmune regulation. At sites of inflammation, acupuncture enables the recruitment of immune cells, causing the release of opioid peptides, while also exerting direct analgesic effects via nerve endings. Furthermore, acupuncture promotes the balance of immune cells and regulates the release of inflammatory factors, thereby reducing the stimulation of nociceptive receptors in peripheral organs. Acupuncture also alleviates peripheral neurogenic inflammation by inhibiting the release of substance P (SP) and calcitonin gene-related peptide from the dorsal root ganglia. At the central nervous system level, acupuncture inhibits the crosstalk between glial cells and neurons by inhibiting the p38 MAPK, ERK, and JNK signaling pathways and regulating the release of inflammatory mediators. It also reduces the excitability of the pain pathway by reducing the release of excitatory neurotransmitters and promoting the release of inhibitory neurotransmitters from neurons and glial cells. In conclusion, the regulation of neuroimmune crosstalk at the peripheral and central levels mediates the anti-inflammatory and analgesic effects of acupuncture on inflammatory pain in an integrated manner. These findings provide novel insights enabling the clinical application of acupuncture in the treatment of inflammatory diseases.

Although pain is regarded as a global public health priority, analgesic therapy remains a significant challenge. Pain is a hypersensitivity state caused by peripheral and central sensitization, with the latter considered the culprit for chronic pain. This study summarizes the pathogenesis of central sensitization from the perspective of neuroglial crosstalk and synaptic plasticity and underlines the related analgesic mechanisms of acupuncture. Central sensitization is modulated by the neurotransmitters and neuropeptides involved in the ascending excitatory pathway and the descending pain modulatory system. Acupuncture analgesia is associated with downregulating glutamate in the ascending excitatory pathway and upregulating opioids, 𝛾-aminobutyric acid, norepinephrine, and 5-hydroxytryptamine in the descending pain modulatory system. Furthermore, it is increasingly appreciated that neurotransmitters, cytokines, and chemokines are implicated in neuroglial crosstalk and associated plasticity, thus contributing to central sensitization. Acupuncture produces its analgesic action by inhibiting cytokines, such as interleukin-1β, interleukin-6, and tumor necrosis factor-α, and upregulating interleukin-10, as well as modulating chemokines and their receptors such as CX3CL1/CX3CR1, CXCL12/CXCR4, CCL2/CCR2, and CXCL1/CXCR2. These factors are regulated by acupuncture through the activation of multiple signaling pathways, including mitogen-activated protein kinase signaling (e.g., the p38, extracellular signal-regulated kinases, and c-Jun-N-terminal kinase pathways), which contribute to the activation of nociceptive neurons. However, the responses of chemokines to acupuncture vary among the types of pain models, acupuncture methods, and stimulation parameters. Thus, the exact mechanisms require future clarification. Taken together, inhibition of central sensitization modulated by neuroglial plasticity is central in acupuncture analgesia, providing a novel insight for the clinical application of acupuncture analgesia.

The acupuncture acupoint is the critical initial site for the therapeutic efficacy of electroacupuncture (EA). Previous studies have confirmed that the NF-κB pathway within the acupoint region mediates the therapeutic effects of acupuncture. Therefore, this study focuses on an in-depth investigation of the MD2/TLR4/NF-κB axis. The mouse model of adjuvant-induced arthritis (AIA) was established via intraplantar injection of Complete Freund's Adjuvant (CFA). EA intervention was applied bilaterally to the Zusanli (ST36) acupoints, and behavioral, molecular, and immunological approaches were integrated to investigate the role of MD2 in EA-mediated analgesia. EA increased paw thermal withdrawal thresholds (PTWTs) in AIA mice ( < 0.05), accompanied by higher levels of MD2, TLR4, p65, and the phosphorylated form of p65 (p-p65) at the acupoint. Co-immunoprecipitation (Co-IP) confirmed binding between MD2 and TLR4 in ST36 acupoint, while immunofluorescence (IF) revealed co-localization of TLR4 with fibroblasts and mast cells in ST36, suggesting these immune cells are critical targets for signal activation. Lentivirus-mediated knockdown of MD2 in the acupoint partially reversed EA's analgesic effects and suppressed downstream TLR4/NF-κB pathway activation, whereas MD2 overexpression elicited a partial analgesic effect and promoted pathway activation. Together with spinal cord proteomics data, these findings indicate that modulating MD2 in the acupoint can regulate spinal cord-related signaling pathways. Mechanistically, EA dynamically regulates the equilibrium of the Grem1/BMP4/COX2 axis in the spinal dorsal horn via activation of the MD2/TLR4/NF-κB pathway cascade, achieving systemic analgesia. This study provides molecular evidence supporting the \"acupoint priming\" theory in acupuncture and highlights MD2 as a potential therapeutic target for pain management.

The metal-plastic flow and bonding strength of three-layer copper (Cu) with single-layer nickel (Ni) joints via ultrasonic welding were investigated in this study. With the increase of welding time from 0.3 to 0.5 s, the weld bonding density between different layers’ interface increased gradually and approached about 95 ± 1.5%. Electron backscatter diffraction (EBSD) analysis of different regions of the welded joint revealed that the metal grains in the 1st layer became relatively small and elongated, while the 2nd and 3rd layers tended to be equiaxed grains. The joint bonding strength of T-peel tests changed with welding time and had two kinds of fracture models (nugget pullout and interfacial fracture). Compared with the bonding strength of the 1st-2nd and 3rd-4th interface, the 2nd-3rd interface of joints had the highest bonding strength of 400.6 N with nugget pullout fracture model at welding time of 0.4 s. In addition, the much higher hardness of the 1st layer is attributed to the strong plastic deformation of the 1st layer, while the dynamic recovery and dynamic recrystallization of the metal of the 2nd layer resulted in the decrease of hardness.

Background Rheumatoid arthritis (RA) is a systemic autoimmune disease that requires multitarget therapeutic strategies. Acupuncture, an integrative therapy of traditional Chinese medicine (TCM), has shown efficacy in the clinical treatment of RA, but its molecular mechanisms remain unclear. Purpose This study systematically elucidated the holistic regulatory effects of acupuncture on RA by integrating network topology with machine learning approaches. Methods Data on the interactions between acupuncture-affected endogenous compounds and RA-related targets were extracted from databases, and a multidimensional interaction network was constructed to map the interactions between acupuncture and RA. screened RA-related differentially expressed genes (DEGs) from the GEOdatabase that intersected with acupuncture-responsive genes. The clusterProfiler was used for KEGG/GO enrichment analysis of these DEGs, and the immune microenvironment was analyzed via the CIBERSORTx and xCell algorithms. ConsensusClusterPlus (R package) was used for unsupervised clustering to obtain DEGs. Subsequently, key genes were identified via an ensemble machine learning model (GLM/SVM/XGB/RF), and nomograms were created. Two-sample MR and colocalization analyses were applied to validate the causal relationship between core acupuncture-affected DEGs and RA risk. Results This study identified 10 acupuncture-regulated endogenous compounds and 49 RA-related DEGs. KEGG analysis revealed that the DEGs enriched in immune pathways included the JAK/STAT pathway, which mediates inflammatory responses, the T-cell receptor signaling pathway, which is involved in T-cell differentiation, and the TNF signaling pathway. Immunome profiling via the CIBERSORT algorithm revealed that the DEGs were enriched primarily in key immune cell subpopulations, such as M1 macrophages, activated CD4⁺ T cells, Tregs, and B lymphocytes. Machine learning identified five key genes associated with immune infiltration (STAT1, GAPDH, JAK2, PTGS2, and MDM2). MR/colocalization confirmed that acupuncture-regulated STAT1 expression was positively correlated with RA genetic susceptibility, highlighting that the STAT1-mediated JAK/STAT pathway is involved in immune remodeling. Conclusion STAT1, GAPDH, JAK2, PTGS2, and MDM2 may be potential targets for the acupuncture treatment of RA. Acupuncture may achieve systemic immune regulation by synergistically targeting multiple pathways (JAK/STAT, TNF) and immune cells (M1 macrophages, CD4 + T cells). This initiative integrates the holistic philosophy of TCM with the precision of AI-driven medical science.

Platinum-based chemotherapy is an effective treatment used in multiple tumor treatments, but produces severe side effects including neurotoxicity, anemia, and immunosuppression, which limits its anti-tumor efficacy and increases the risk of infections. Electroacupuncture (EA) is often used to ameliorate these side effects, but its mechanism is unknown. Here, we report that EA on ST36 and SP6 prevents cisplatin-induced neurotoxicity and immunosuppression. EA induces neuroprotection, prevents pain-related neurotoxicity, preserves bone marrow (BM) hematopoiesis, and peripheral levels of leukocytes. EA activates sympathetic BM terminals to release pituitary adenylate cyclase activating polypeptide (PACAP). PACAP-receptor PAC1-antagonists abrogate the effects of EA, whereas PAC1-agonists mimic EA, prevent neurotoxicity, immunosuppression, and preserve BM hematopoiesis during cisplatin chemotherapy. Our results indicate that PAC1-agonists may provide therapeutic advantages during chemotherapy to treat patients with advanced neurotoxicity or neuropathies limiting EA efficacy.

The sandstone sections in the Upper Jurassic red beds of the Yongjin area in the central Junggar Basin are important oil and gas reservoirs. The debate over whether red beds are of primary depositional or secondary diagenetic origin persists, leading to uncertainties in the interpretation of reservoir sedimentary facies. This study uses core samples and employs thin section microscope observations, scanning electron microscopy, X-ray diffraction, and major and trace element analyses to investigate the formation period and paleoclimate conditions of red beds and explore the origin of red sandstone. The Upper Jurassic red beds are mainly deposited in arid delta plain environments. The framework grains of the red sandstone are composed of quartz (averaging 22.6%), feldspar (averaging 16.3%), and rock fragments (averaging 36.7%). The rock fragments in the sandstone are mainly composed of intermediate basic volcanic rocks and cryptocrystalline acid volcanic rocks, which are rich in mafic silicate minerals such as olivine, pyroxene, ilmenite, and magnetite. In situ hematitization of ilmenite is observed in the rock fragments, suggesting that the in situ alteration of mafic silicate minerals in the parent rock is the main source of iron ions for hematite. Tiny hematite crystals (2.1 μm) are observed in clay mineral micropores via SEM. Abundant mixed-layer illite/smectite clay indicates early smectite transformation, providing a minor source of iron ions for hematite. Hematite in the red sandstone occurs as a grain-coating type, predating quartz overgrowth, feldspar overgrowth, and (ferroan) calcite and (ferroan) dolomite precipitation. Residual hematite coatings between detrital grain point contacts indicate that hematite is a product of syn-sedimentary or very early diagenetic precipitation, ruling out the possibility that red sandstone formation was caused by later atmospheric water leaching during the fold and thrust belt stage. The average chemical index of alteration (CIA) for the red sandstone is 52.2, whereas the CIA for the red mudstone averages 59.5, and the chemical index of weathering (CIW) reached a maximum of 69. These values indicate that the rocks have undergone mild chemical weathering in arid climates. Additionally, the ratios of trace elements indicate that the water bodies were in an oxidizing state during the sedimentary period. The arid climate and oxidative water conditions were ideal for hematite preservation, thus facilitating red bed formation. The red bed sediments in the study area represent a direct response to the Late Jurassic aridification event and can be compared to global climate change. The results have important implications for stratigraphic correlation and interpretation of reservoir sedimentary facies in the study area while also providing a valuable case study for global research on red beds.