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Autoimmune diseases are a worldwide health problem with growing rates of morbidity, and are characterized by breakdown and dysregulation of the immune system. Although their etiology and pathogenesis remain unclear, the application of dietary supplements is gradually increasing in patients with autoimmune diseases, mainly due to their positive effects, relatively safety, and low cost. Quercetin is a natural flavonoid that is widely present in fruits, herbs, and vegetables. It has been shown to have a wide range of beneficial effects and biological activities, including anti-inflammation, anti-oxidation, and neuroprotection. In several recent studies quercetin has reportedly attenuated rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, and systemic lupus erythematosus in humans or animal models. This review summarizes the evidence for the pharmacological application of quercetin for autoimmune diseases, which supports the view that quercetin may be useful for their prevention and treatment.

Background Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies worldwide because of rapid progression and high incidence of metastasis or recurrence. Accumulating evidence shows that CD73-expressing tumor cell is implicated in development of several types of cancer. However, the role of CD73 in HCC cell has not been systematically investigated and its underlying mechanism remains elusive. Methods CD73 expression in HCC cell was determined by RT-PCR, Western blot, and immunohistochemistry staining. Clinical significance of CD73 was evaluated by Cox regression analysis. Cell counting kit-8 and colony formation assays were used for proliferation evaluation. Transwell assays were used for motility evaluations. Co-immunoprecipitation, cytosolic and plasma membrane fractionation separation, and ELISA were applied for evaluating membrane localization of P110β and its catalytic activity. NOD/SCID/γc(null) (NOG) mice model was used to investigate the in vivo functions of CD73. Results In the present study, we demonstrate that CD73 was crucial for epithelial-mesenchymal transition (EMT), progression and metastasis in HCC. CD73 expression is increased in HCC cells and correlated with aggressive clinicopathological characteristics. Clinically, CD73 is identified as an independent poor prognostic indicator for both time to recurrence and overall survival. CD73 knockdown dramatically inhibits HCC cells proliferation, migration, invasion, and EMT in vitro and hinders tumor growth and metastasis in vivo. Opposite results could be observed when CD73 is overexpressed. Mechanistically, adenosine produced by CD73 binds to adenosine A2A receptor (A2AR) and activates Rap1, which recruits P110β to the plasma membrane and triggers PIP3 production, thereby promoting AKT phosphorylation in HCC cells. Notably, a combination of anti-CD73 and anti-A2AR achieves synergistic depression effects on HCC growth and metastasis than single agent alone. Conclusions CD73 promotes progression and metastasis through activating PI3K/AKT signaling, indicating a novel prognostic biomarker for HCC. Our data demonstrate the importance of CD73 in HCC in addition to its immunosuppressive functions and revealed that co-targeting CD73 and A2AR strategy may be a promising novel therapeutic strategy for future HCC management.

Accumulated reactive oxygen species (ROS) directly contribute to biomacromolecule damage and influence various inflammatory responses. Reactive oxygen species act as mediator between innate and adaptive immune cells, thereby influencing the antigen-presenting process that results in T cell activation. Evidence from patients with chronic granulomatous disease and mouse models support the function of ROS in preventing abnormal autoimmunity; for example, by supporting maintenance of macrophage efferocytosis and T helper 1/T helper 2 and T helper 17/ regulatory T cell balance. The failure of many anti-oxidation treatments indicates that ROS cannot be considered entirely harmful. Indeed, enhancement of ROS may sometimes be required. In a mouse model of rheumatoid arthritis (RA), absence of NOX2-derived ROS led to higher prevalence and more severe symptoms. In patients with RA, naïve CD4 + T cells exhibit inhibited glycolysis and enhanced pentose phosphate pathway (PPP) activity, leading to ROS exhaustion. In this “reductive” state, CD4 + T cell immune homeostasis is disrupted, triggering joint destruction, together with oxidative stress in the synovium.

The morbidity and mortality of autoimmune diseases (Ads) have been increasing worldwide, and the identification of novel therapeutic strategies for prevention and treatment is urgently needed. Sirtuin 1 (SIRT1), a member of the class III family of nicotinamide adenine dinucleotide (NAD + )-dependent histone deacetylases, has been reported to participate in the progression of several diseases. SIRT1 also regulates inflammation, oxidative stress, mitochondrial function, immune responses, cellular differentiation, proliferation and metabolism, and its altered functions are likely involved in Ads. Several inhibitors and activators have been shown to affect the development of Ads. SIRT1 may represent a novel therapeutic target in these diseases, and small molecules or natural products that modulate the functions of SIRT1 are potential therapeutic agents. In the present review, we summarize current studies of the biological functions of SIRT1 and its role in the pathogenesis and treatment of Ads.

Despite advancements in treatment, the overall mortality rate among critically ill coronary artery disease (CAD) patients remains high. The impact of blood pressure variability (BPV) on these patients remains controversial. This study investigates the relationship between 24-hour BPV and mortality in critically ill CAD patients in the ICU. A retrospective analysis was conducted on CAD patients admitted to the ICU from 2008 to 2019 using the MIMIC-IV database. BPV was assessed by calculating average real variability (ARV) during the first 24 h of ICU admission, classifying patients into low, medium, and high ARV groups. Endpoints included in-hospital and 1-year mortality, analyzed using logistic regression, Cox proportional hazards regression, and restricted cubic splines. A total of 4,588 CAD patients were included. ARV of diastolic blood pressure (DBP) was positively correlated with 1-year mortality (HR 1.03, 95% CI 1.00-1.06), independent of other factors. ARVof systolic blood pressure (SBP) showed a U-shaped relationship with 1-year mortality; values below 16.912 mmHg reduced risk (HR 0.956, 95% CI 0.924–0.988), while higher values increased risk (HR 1.180, 95% CI 1.044–1.333). No significant associations were found with short-term mortality. In critically ill CAD patients, 24-hour ARV of DBP and SBP show significant associations with 1-year mortality. Elevated DBP variability is associated with increased risk, while SBP variability demonstrates a U-shaped association, suggesting both very low and very high SBP variability are detrimental. These findings highlight the potential importance of monitoring BPV to identify high-risk patients and suggest that targeted BP management strategies, considering variability, may improve long-term outcomes.

As a mature non-destructive testing technology, near-infrared (NIR) spectroscopy can effectively identify and distinguish the structural characteristics of wood. The Wood Defect One-Dimensional Visual Geometry Group 19-Finite Element Analysis (WD-1D-VGG19-FEA) algorithm is used in this study. 1D-VGG19 classifies the near-infrared spectroscopy data to determine the knot area, fiber deviation area, transition area, and net wood area of the solid wood board surface and generates a two-dimensional image of the board surface through inversion. Then, the nonlinear three-dimensional model of wood with defects was established by using the inverse image, and the finite element analysis was carried out to predict the elastic modulus of wood. In the experiment, 270 points were selected from each of the four regions of the wood, totaling 1080 sets of near-infrared data, and the 1D-VGG19 model was used for classification. The results showed that the identification accuracy of the knot area was 95.1%, the fiber deviation area was 92.7%, the transition area was 90.2%, the net wood area was 100%, and the average accuracy was 94.5%. The error range of the elastic modulus prediction of the three-dimensional model established by the VGG19 classification model in the finite element analysis is between 2% and 10%, the root mean square error (RMSE) is about 598. 2, and the coefficient of determination (R2) is 0. 91. This study shows that the combination of the VGG19 algorithm and finite element analysis can accurately describe the nonlinear defect morphology of wood, thus establishing a more accurate prediction model of wood mechanical properties to maximize the use of wood mechanical properties.

Strontium ferrite nanoparticles were prepared by a coprecipitation method, and reduced graphene oxide/strontium ferrite/polyaniline (R-GO/SF/PANI) ternary nanocomposites were prepared by in situ polymerization method. The morphology, structure, and magnetic properties of the ternary nanocomposites were investigated by X-ray powder diffraction (XRD), Fourier transform infrared spectroscopy (FT-IR), TEM, Raman, and VSM. The microwave-absorbing properties of the composites were measured by a vector network analyzer. The XRD patterns show the single phase of strontium hexaferrite without other intermediate phases. TEM photographs reveal that strontium ferrite nanoparticles are uniformly dispersed on the surfaces of R-GO sheets. The R-GO/SF/PANI nanocomposite exhibited the best absorption property with the optimum matching thickness of 1.5 mm in the frequency of 2–18 GHz. The value of the maximum RL was −45.00 dB at 16.08 GHz with the 5.48-GHz bandwidth. The excellent absorption properties of R-GO/SF/PANI nanocomposites indicated their great potential as microwave-absorbing materials.

The deformation and failure forms of inclined coal seam roadway under the joint action of dip angle and various geological conditions are complex, and there is a lack of targeted support measures, which brings great problems to the stability control of roadway surrounding rock. In order to safely and economically mine inclined coal seams, taking the engineering geology of Shitanjing No. 2 mining area as the background, and the physical similarity model of right-angle trapezoidal roadway in inclined coal seam, in which the non-contact digital image correlation (DIC) technology and the stress sensor is employed to provide full-field displacement and stress measurements. The deformation control technology of the roadway surrounding rock was proposed, verified by numerical simulation and applied to engineering practice. The research results show that the stress and deformation failure of surrounding rock in low sidewall of roadway are greater than those in high sidewall, showing asymmetric characteristics, and the maximum stress concentration coefficients of roadway sidewall, roof and floor are 4.1, 3.4 and 2.8, respectively. A concept of roadway \"cyclic failure\" mechanism is proposed that is, the cyclic interaction of the two sidewalls, the sharp angles and roof aggravated the failure of roadway, resulting in the overall instability of roadway. The roadway sidewall is serious rib spalling, the roof is asymmetric \"Beret\" type caving arch failure, and the floor is slightly bulging. On this basis, the principle of roadway deformation control is revealed and asymmetric support design is adopted, and the deformation of roadway is controlled, which support scheme is effective.

Rheumatoid arthritis (RA) is an autoimmune inflammatory disease, of which the leading cause of death is cardiovascular disease (CVD). The levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), and high-density lipoprotein cholesterol (HDL-c) in RA decrease especially under hyperinflammatory conditions. It is conflictive with the increased risk of CVD in RA, which is called “lipid paradox”. The systemic inflammation may explain this apparent contradiction. The increased systemic proinflammatory cytokines in RA mainly include interleukin-6(IL-6)、interleukin-1(IL-1)and tumor necrosis factor alpha(TNF-α). The inflammation of RA cause changes in the subcomponents and structure of HDL particles, leading to a weakened anti-atherosclerosis function and promoting LDL oxidation and plaque formation. Dysfunctional HDL can further worsen the abnormalities of LDL metabolism, increasing the risk of cardiovascular disease. However, the specific mechanisms underlying lipid changes in RA and increased CVD risk remain unclear. Therefore, this article comprehensively integrates the latest existing literature to describe the unique lipid profile of RA, explore the mechanisms of lipid changes, and investigate the impact of lipid changes on cardiovascular disease.

Background: Wutou Decoction (WTD), as a classic prescription, has been generally used to treat rheumatoid arthritis (RA) for two thousand years in China. However, the potential protective effects of WTD on rheumatoid arthritis and its possible mechanism have rarely been reported. Purpose: The aim of this study was to explore the possible mechanism of WTD against RA and a promising alternative candidate for RA therapy. Methods: A model of collagen-induced arthritis (CIA) was constructed in rats to assess the therapeutic effects of WTD. Histopathological staining, immunofluorescence, and western blotting of synovial sections were conducted to detect the antiangiogenic effects of WTD. Then, cell viability assays, flow cytometry, scratch healing assays, and invasion assays were conducted to explore the effects of WTD on MH7A human fibroblast-like synoviocyte (FLS) cell proliferation, apoptosis, migration, and invasion in vitro . The ability of WTD to induce blood vessel formation after MH7A cell and human umbilical vein endothelial cell line (HUVEC) coculture with WTD intervention was detected by a tube formation assay. The mechanisms of WTD were screened by network pharmacology and confirmed by in vivo and in vitro experiments. Results: WTD ameliorated the symptoms and synovial pannus hyperplasia of CIA rats. Treatment with WTD inhibited MH7A cell proliferation, migration, and invasion and promoted MH7A apoptosis. WTD could inhibit MH7A cell expression of proangiogenic factors, including VEGF and ANGI, to induce HUVEC tube formation. Furthermore, the PI3K-AKT-mTOR-HIF-1α pathway was enriched as a potential target of WTD for the treatment of RA through network pharmacology enrichment analysis. Finally, it was confirmed in vitro and in vivo that WTD inhibits angiogenesis in RA by interrupting the PI3K-AKT-mTOR-HIF-1α pathway. Conclusion: WTD can inhibit synovial hyperplasia and angiogenesis, presumably by inhibiting the migration and invasion of MH7A cells and blocking the production of proangiogenic effectors in MH7A cells. The possible underlying mechanism by which WTD ameliorates angiogenesis in RA is the PI3K-AKT-mTOR-HIF-1α pathway.