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This study investigates the impact of different temperatures and initial Mg2+/Ca2+ molar ratios in the solution on the wet-accelerated carbonation of β-dicalcium silicate (β-C2S). The x-ray diffraction (XRD), fourier transform infrared spectroscopy (FT-IR), thermogravimetric analyzer (TGA), and field emission scanning electron microscopy (FE-SEM) analysis results indicated that temperature and the Mg2+/Ca2+ molar ratio are key factors in the nucleation of aragonite. Aragonite formed at a temperature above 60 °C, and the high temperature promoted the crystallinity of needle-like aragonite with a length of 1–6 μm and a diameter of ~1 μm. Moreover, 80 °C was the most favorable temperature for the formation of aragonite with a large aspect ratio in the carbonation system of β-C2S. Mg2+ had a significant effect on inhibiting the transformation of aragonite to calcite and promoting the stability of aragonite. Aragonite became the dominant CaCO3 polymorph instead of calcite when the Mg2+/Ca2+ molar ratio was above 1.0, and pure aragonite-style calcium carbonate was formed at a Mg2+/Ca2+ molar ratio of 1.5.

Chronic stress is a key risk factor for depression, and microglia have been implicated in the pathogenesis of the disease. Recent studies show that the Nod-like receptor protein 3 (NLRP3) inflammasome is expressed in microglia and may play a crucial role in depression. However, the mechanism of NLRP3 inflammasome activation in hippocampal microglia and its role in depressive-like behaviors remain poorly understood. In this study, rats were subjected to 6 h of restraint stress per day for 21 days to produce a model of stress-induced depression. Behavioral tests and serum corticosterone were used to assess the success of the model. Furthermore, HAPI cells were pretreated with dexamethasone (5 × 10-7 M) to assess stress-induced changes in microglial cells in culture. The microglial marker Iba-1, reactive oxygen species (ROS), nuclear factor kappa B (NF-κB) and key components of the NLRP3 inflammasome and its downstream inflammatory effectors (IL-1β and IL-18) were measured. Chronic stress induced depressive-like behavior, increased serum corticosterone levels and produced hippocampal structural changes. Chronic stress and dexamethasone both increased Iba-1 expression and ROS formation and also elevated levels of NF-κB, NLRP3, cleaved caspase-1, IL-1β and IL-18. After use of the NF-κB inhibitor BAY 117082 and knocked out NLRP3 in vitro decreased ROS formation and the expression of Iba-1, NF-κB and NLRP3 as well as levels of cleaved caspase-1, IL-1β and IL-18. These findings suggest that activation of the glucocorticoid receptor-NF-κB-NLRP3 pathway in hippocampal microglia mediates chronic stress-induced hippocampal neuroinflammation and depression-like behavior.

Fever has long been recognized as one of the earliest clinical indicators of illness and remains a leading reason for seeking medical care worldwide. It is typically classified based on its duration and underlying etiology. In clinical settings, intractable fever is as common as acute fever, particularly in patients with brain injuries. Beyond infectious causes, stroke survivors often experience recurrent intractable fever due to central or neurogenic mechanisms. This study aims to retrospectively investigate the incidence and clinical characteristics of acute and intractable fever in patients undergoing stroke rehabilitation. It explores the associations between these characteristics and the different types of fever. Additionally, the study seeks to identify potential risk factors contributing to the development of intractable fever, aiming to guide clinical management and optimize treatment strategies for stroke-related fever. This study evaluated 1,065 stroke patients in the rehabilitation phase who were admitted to the Neurorehabilitation Center between January 1, 2023, and December 31, 2023. Of these, 230 febrile patients met the inclusion criteria and were included in the analysis, comprising 194 cases of acute fever and 36 cases of intractable fever. Medical records and clinical characteristics were collected, and the data from the two groups of febrile patients were analyzed using t-tests, Mann-Whitney U tests, and chi-square tests. Logistic regression analysis was performed to identify risk factors associated with intractable fever, while receiver operating characteristic (ROC) curves were used to assess the predictive performance of individual and combined risk factors. A p-value of less than 0.05 was considered statistically significant. 15.7% of patients experienced intractable fever, which was significantly associated with brainstem lesions ( P  < 0.05). Compared to patients with acute fever, those with intractable fever had higher NIHSS scores (33.3% vs. 15.5%, P  < 0.05), a greater incidence of consciousness disorders (66.7% vs. 28.9%, P  < 0.05), and a higher rate of tracheostomy (55.6% vs. 15.5%, P  < 0.05). All patients received antibiotic treatment, and gabapentin was administered to 16 cases. Patients with brainstem lesions were less likely to be treated with gabapentin (37.5% vs. 90%, P  < 0.05), while those with intracerebral hemorrhage were more likely to receive gabapentin (87.5% vs. 10%, P  < 0.05). Logistic regression analysis revealed that consciousness disorders and tracheostomy status were significant risk factors for intractable fever ( P  = 0.047, OR 6.691, 95% CI 1.030–43.478; P  = 0.021, OR 5.366, 95% CI 1.282–22.465). Brainstem lesions also significantly increased the risk ( P  = 0.002, OR 9.617, 95% CI 2.277–40.614). Although limited in scope, this retrospective study highlights the increased risk of intractable fever during stroke rehabilitation among patients with consciousness disorders, tracheostomy, and brainstem injuries. The key risk factors identified include higher NIHSS scores, impaired consciousness, tracheostomy status, and brainstem lesions.

Due to the complexity of the automobile manufacturing process, some flexible and delicate assembly work relies on manual operations. However, high-frequency and high-load repetitive operations make assembly workers prone to physical fatigue. This study proposes a method for evaluating human physical fatigue for the manual assembly of automobiles with methods: NIOSH (National Institute for Occupational Safety and Health), OWAS (Ovako Working Posture Analysis System) and RULA (Rapid Upper Limb Assessment). The cerebral oxygenation signal is selected as an objective physiological index reflecting the human fatigue level to verify the proposed physical fatigue evaluation method. Taking auto seat assembly and automobile manual assembly as an example, 18 group experiments were carried out with the ARE platform (Augmented Reality-based Ergonomic Platform). Furthermore, predictions of metabolic energy expenditure were performed for experiments in Tecnomatix Jack. Finally, it is concluded that the proposed physical fatigue evaluation method can reflect the human physical fatigue level and is more accurate than the evaluation of metabolic energy consumption in Tecnomatix Jack because of the immersion that comes with the AR devices and the precision that comes with motion capture devices.

Background Tuberculosis (TB) represents a bacterial infection affecting many individuals each year and potentially leading to death. Overexpression of transforming growth factor (TGF)-β1 has a primary immunomodulatory function in human tuberculosis. This work aimed to develop nanoliposomes to facilitate the delivery of anti-tubercular products to THP-1-derived human macrophages as Mycobacterium host cells and to evaluate drug efficiencies as well as the effects of a TGF-β1-specific short interfering RNA (siRNA) delivery system employing nanoliposomes. Methods In the current study, siTGF-β1 nanoliposomes loaded with the anti-TB drugs HRZ (isoniazid, rifampicin, and pyrazinamide) were prepared and characterized in vitro, determining the size, zeta potential, morphology, drug encapsulation efficiency (EE), cytotoxicity, and gene silencing efficiency of TGF-β1 siRNA. Results HRZ/siTGF-β1 nanoliposomes appeared as smooth spheres showing the size and positive zeta potential of 168.135 ± 0.5444 nm and + 4.03 ± 1.32 mV, respectively. Drug EEs were 90%, 88%, and 37% for INH, RIF, and PZA, respectively. Meanwhile, the nanoliposomes were weakly cytotoxic towards human macrophages as assessed by the MTT assay. Nanoliposomal siTGF-β1 could significantly downregulate TGF-β1 in THP-1-derived human macrophages in vitro. Conclusion These findings suggested that HRZ-loaded nanoliposomes with siTGF-β1 have the potential for improving spinal tuberculosis chemotherapy via nano-encapsulation of anti-TB drugs.

Ground source heat pump (GSHP) system, which extracts underground heat for building heating and cooling, uses renewable energy to decrease CO2 emissions for the goals of carbon peaking and carbon neutrality. Hence, the prediction and optimization work is significate especially for existing GSHP system. This study focuses on the prediction of heat extraction and optimization of operational strategy based on a three-story house installed with GSHP system located in Cleveland, Ohio, USA. Firstly, the numerical model is built to simulate operation of ground heat exchanger (GHE). Then, Latin hypercube sampling (LHS) is employed to generate different parameter combinations that are calculated to get the heat extraction results for training XGBoost-based surrogate model. Finally, the particle swarm optimization (PSO) is used to realize the optimization of operational strategy. The results indicate that the numerical model can simulate the GHE well, and the accuracy of surrogate model can reach 0.990. The COP of GSHP system is maximized to protect the soil heat balance and reduce the electrical energy consumption. The optimization method also makes it possible to evaluate the heat extraction capability, and prepare for the extra heat demand in advance.

In recent years, the ethylene-mediated ripening and softening of non-climacteric fruits have been widely mentioned. In this paper, recent research into the ethylene-mediated ripening and softening of non-climacteric fruits is summarized, including the involvement of ethylene biosynthesis and signal transduction. In addition, detailed studies on how ethylene interacts with other hormones to regulate the ripening and softening of non-climacteric fruits are also reviewed. These findings reveal that many regulators of ethylene biosynthesis and signal transduction are linked with the ripening and softening of non-climacteric fruits. Meanwhile, the perspectives of future research on the regulation of ethylene in non-climacteric fruit are also proposed. The overview of the progress of ethylene on the ripening and softening of non-climacteric fruit will aid in the identification and characterization of key genes associated with ethylene perception and signal transduction during non-climacteric fruit ripening and softening.

Anti-cancer immunity and response to immune therapy is influenced by the metabolic states of the tumours. Immune checkpoint blockade therapy (ICB) is known to involve metabolic adaptation, however, the mechanism is not fully known. Here we show, by metabolic profiling of plasma samples from melanoma-bearing mice undergoing anti-PD1 and anti-CTLA4 combination therapy, that higher levels of purine metabolites, including inosine, mark ICB sensitivity. Metabolic profiles of ICB-treated human cancers confirm the association between inosine levels and ICB sensitivity. In mouse models, inosine supplementation sensitizes tumours to ICB, even if they are intrinsically ICB resistant, by enhancing T cell-mediated cytotoxicity and hence generating an immunologically hotter microenvironment. We find that inosine directly inhibits UBA6 in tumour cells, and lower level of UBA6 makes the tumour more immunogenic and this is reflected in favourable outcome following ICB therapy in human melanomas. Transplanted mouse melanoma and breast cancer cells with genetic ablation of Uba6 show higher sensitivity to ICB than wild type tumours. Thus, we provide evidence of an inosine-regulated UBA6-dependent pathway governing tumour-intrinsic immunogenicity and hence sensitivity to immune checkpoint inhibition, which might provide targets to overcome ICB resistance. The metabolic environment of tumours has wide-ranging effects on the anti-tumour immune response and the outcome of immune therapy. Authors show here that the purine metabolite inosine enhances tumour immunogenicity and thus immune checkpoint blockade therapy response by inhibiting the ubiquitin-activating enzyme UBA6 in tumour cells.

Acute kidney injury (AKI) is often secondary to sepsis. Previous studies suggest that damaged mitochondria and the inhibition of autophagy results in AKI during sepsis, but dexmedetomidine (DEX) alleviates lipopolysaccharide (LPS)-induced AKI. However, it is uncertain whether the renoprotection of DEX is related to autophagy or the clearance of damaged mitochondria in sepsis-induced AKI. In this study, AKI was induced in rats by injecting 10 mg/kg of LPS intraperitoneally (i.p.). The rats were also pretreated with DEX (30 μg/kg, i.p.) 30 min before the injection of LPS. The structure and function of kidneys harvested from the rats were evaluated, and the protein levels of autophagy-related proteins, oxidative stress levels, and apoptosis levels were measured. Further, atipamezole (Atip) and 3-Methyladenine (3-MA), which are inhibitors of DEX and autophagy, respectively, were administered before the injection of DEX to examine the protective mechanism of DEX. Pretreatment with DEX ameliorated kidney structure and function. DEX decreased the levels of blood urea nitrogen (BUN) and creatinine (Cre), urine kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), reactive oxygen species (ROS), and apoptosis proteins (such as cleaved caspase-9 and cleaved caspase-3). However, DEX upregulated the levels of autophagy and mitophagy proteins, such as Beclin-1, LC3 II and PINK1. These results suggest that DEX ameliorated LPS-induced AKI by reducing oxidative stress and apoptosis and enhancing autophagy. To promote autophagy, DEX inhibited the phosphorylation levels of PI3K, AKT, and mTOR. Furthermore, the administration of Atip and 3-MA inhibitors blocked the renoprotection effects of DEX. Here, we demonstrate a novel mechanism in which DEX protects against LPS-induced AKI. DEX enhances autophagy, which results in the removal of damaged mitochondria and reduces oxidative stress and apoptosis in LPS-induced AKI through the α -AR and inhibition of the PI3K/AKT/mTOR pathway.

Nitrogen (N) is an essential element for plant growth, development, and metabolism. In apple production, the excessive use of N fertilizer may cause high N stress. Whether high N stress can be alleviated by regulating melatonin supply is unclear. The effects of melatonin on root morphology, antioxidant enzyme activity and 13 C and 15 N accumulation in apple rootstock M9T337 treated with high N were studied by soil culture. The results showed that correctly raising the melatonin supply level is helpful to root development of M9T337 rootstock under severe N stress. Compared with HN treatment, HN+MT treatment increased root and leaf growth by 11.38%, and 28.01%, respectively. Under high N conditions, appropriately increasing melatonin level can activate antioxidant enzyme activity, reduce lipid peroxidation in roots, protect root structural integrity, promote the transport of sorbitol and sucrose to roots, and promote further degradation and utilization of sorbitol and sucrose in roots, which is conducive to the accumulation of photosynthetic products, thereby reducing the inhibitory effect of high N treatment on root growth. Based on the above research results, we found that under high N stress, melatonin significantly promotes nitrate absorption, enhances N metabolism enzyme activity, and upregulates related gene expression, and regulate N uptake and utilization in the M9T337 rootstock. These results presented a fresh notion for improving N application and preserving carbon-nitrogen balance.