Algorithm for diagnosing and warning of vibration caused by loosened screws on motor base using wavelet packet and neural network.

Motor base screw loosening is a common problem in motor operation, which, if not dealt with in time, may lead to motor failure and damage. However, few studies have focused on the diagnosis and warning of this problem. Based on wavelet packet and neural network analysis, this paper presents a new algorithm for monitoring, diagnosing, and warning vibration caused by loose screws in the motor base. The vibration signal generated by the base screw loosening is monitored and sampled with sensors, and the wavelet packet is used to decompose, reconstruct, and reduce the noise of the vibration signal to enhance the time-frequency characteristics of the signal. After analyzing the fault data by wavelet, the feature vector characterizing the fault is extracted, and then, the vector and the corresponding fault type are used as the input and output of the neural network, respectively, and the non-mapping relationship between them is built to complete the diagnosis and early warning of the fault. Finally, the method is used to compare the motor base screw loosening operation and normal operation. The experiments show that the new algorithm based on wavelet packet and neural network can complete the health diagnosis and early warning of motor in the early stage of motor base screw loosening, reduce the loss caused by subsequent faults, and provide a new reference scheme for the motor fault diagnosis field.

Elucidating the Volcanic-Type Catalytic Behavior in Lithium-Sulfur Batteries via Defect Engineering.

Defects are generally considered to be effective and flexible in the catalytic reactions of lithium-sulfur batteries. However, the influence of the defect concentration on catalysis remains ambiguous. In this work, molybdenum sulfide with different sulfur vacancy concentrations is comprehensively modulated, showing that the defect level and the adsorption-catalytic performance result in a volcano relationship. Moreover, density functional theory and in situ experiments reveal that the optimal level of sulfur defects can effectively increase the binding energy between molybdenum sulfide and lithium polysulfides (LiPSs), lower the energy barrier of the LiPS conversion reaction, and promote the kinetics of Li2S bidirectional catalytic reaction. The lower bidirectional catalytic performance incited by excessive or deficient sulfur defects is mainly due to the deformed geometrical structures and reduced adsorption of key LiPSs on the catalyst surface. This work underscores the imperative of controlling the defect content and provides a potential approach to the commercialization of lithium-sulfur batteries.

Exercise combined with heat treatment improves insulin resistance in diet-induced obese rats.

Insulin resistance is a risk factor for various cardiovascular diseases, which seriously threaten human health. Thus, finding a safe, effective and economical strategy to treat insulin resistance is urgently needed. This study aimed to investigate the effects of exercise combined with heat treatment on the insulin sensitivity in skeletal muscle of diet-induced obese (DIO) rats. Obese rats were induced by a 10-week high-fat diet and were randomly divided into normal temperature + control (NC), normal temperature + exercise (NE), heat treatment + control (HC) and heat treatment + exercise (HE) groups for 7 weeks of incremental load endurance exercise and heat treatment (exposure to a high-temperature environment room). At the end of the 7-week intervention, we measured fasting blood glucose, serum fasting insulin, serum leptin, serum adiponectin, protein expression of HSF1/HSP27 and JAK2/STAT3 pathway in soleus (primarily composed of slow-twitch fibres) and extensor digitorum longus (primarily composed of fast-twitch fibres) muscles. The results showed that exercise combined with heat treatment can effectively improve insulin resistance by regulating HSF1/HSP27 and JAK2/STAT3 pathways in the slow-twitch muscle of DIO rats. Importantly, exercise combined with heat treatment is more effective in improving insulin resistance in DIO rats than exercise or heat treatment alone. Low-moderate intensity exercise that stimulates slow-twitch muscle, combined with heat treatment is an effective strategy to treat insulin resistance.

Toxic effects of isofenphos-methyl on zebrafish embryonic development.

Isofenphos-methyl (IFP) is widely used as an organophosphorus for controlling underground insects and nematodes. However, excessive use of IFP may pose potential risks to the environment and humans, but little information is available on its sublethal toxicity to aquatic organisms. To address this knowledge gap, the current study exposed zebrafish embryos to 2, 4, and 8 mg/L IFP within 6-96 h past fertilization (hpf) and measured mortality, hatching, developmental abnormalities, oxidative stress, gene expressions, and locomotor activity. The results showed that IFP exposure reduced the rates of heart and survival rate, hatchability, and body length of embryos and induced uninflated swim bladder and developmental malformations. Reduction in locomotive behavior and inhibition of AChE activity indicated that IFP exposure may induce behavioral defects and neurotoxicity in zebrafish larvae. IFP exposure also led to pericardial edema, longer venous sinus-arterial bulb (SV-BA) distance, and apoptosis of the heart cells. Moreover, IFP exposure increased the accumulation of reactive oxygen species (ROS) and the content of malonaldehyde (MDA), also elevated the levels of antioxidant enzymes of superoxide dismutase (SOD) and catalase (CAT), but decreased glutathione (GSH) levels in zebrafish embryos. The relative expressions of heart development-related genes (nkx2.5, nppa, gata4, and tbx2b), apoptosis-related genes (bcl2, p53, bax, and puma), and swim bladder development-related genes (foxA3, anxa5b, mnx1, and has2) were significantly altered by IFP exposure. Collectively, our results indicated that IFP induced developmental toxicity and neurotoxicity to zebrafish embryos and the mechanisms may be relevant to the activation of oxidative stress and reduction of acetylcholinesterase (AChE) content.

The involvement and therapeutic potential of lncRNA Kcnq1ot1/miR-34a-5p/Sirt1 pathway in arsenic trioxide-induced cardiotoxicity.

BACKGROUND/AIMS: Arsenic trioxide (ATO) is the first-line therapeutic drug for acute promyelocytic leukemia. However, the cardiotoxicity of ATO limits its clinical application. This study aims to explore the long noncoding RNA (lncRNA) involved molecular mechanism in ATO-induced cardiotoxicity and to identify available prevention strategies. METHODS: ATO was administered to mice or primary cultured mouse cardiomyocytes. Small interfering RNA targeting lncRNA Kcnq1ot1 (si-Kcnq1ot1) was used to knockdown lncRNA Kcnq1ot1. MiR-34a-5p mimic and antisense morpholino oligonucleotide targeting miR-34a-5p (AMO-34a-5p) were used to upregulate and downregulate the expression of miR-34a-5p, respectively. TUNEL staining was conducted to detect cell DNA damage. Flow cytometry assay was used to detect cell apoptosis. Western blot was conducted to detect Bcl-2, Bax and Sirt1 protein expression. Real-time PCR was used to detect lncRNA Kcnq1ot1, miR-34a-5p, and Sirt1 mRNA expression. Dual-luciferase reporter assay was performed to validate the predicted binding site. RESULTS: ATO induced apoptosis in cardiomyocytes both in vivo and in vitro. Simultaneously, the expression of lncRNA Kcnq1ot1 and Sirt1 was downregulated, and miR-34a-5p was upregulated. MiR-34a-5p has binding sites with lncRNA Kcnq1ot1 and Sirt1. Knockdown of lncRNA Kcnq1ot1 induced apoptosis of cardiomyocytes, with increased miR-34a-5p and decreased Sirt1 expression. Inhibition of miR-34a-5p attenuated si-Kcnq1ot1-induced apoptosis in cardiomyocytes. Therefore, the lncRNA Kcnq1ot1/miR-34a-5p/Sirt1 signaling pathway is involved in ATO-induced cardiotoxicity. Propranolol alleviated ATO-induced apoptosis in cardiomyocytes both in vivo and in vitro, which was related to the lncRNA Kcnq1ot1/miR-34a-5p/Sirt1 signaling pathway. CONCLUSION: The lncRNA Kcnq1ot1/miR-34a-5p/Sirt1 pathway is involved in ATO-induced cardiotoxicity. Propranolol can attenuate ATO-induced cardiotoxicity at least partially through the lncRNA Kcnq1ot1/miR-34a-5p/Sirt1 pathway. Combined administration with propranolol may be a new strategy for alleviating the cardiotoxicity of ATO.

Research progress on ferroptosis in the treatment of oral cancer / 口腔疾病防治

@#Ferroptosis is a newly discovered method of programmed cell death. Current studies have shown that activation of ferroptosis-related pathways can inhibit the growth and proliferation of tumor cells and reverse their drug resistance. Oral cancer is a common malignant tumor with a high recurrence rate and high drug resistance. Inducing ferroptosis is a potential treatment strategy. There are still many uncertainties in the application of ferroptosis in the treatment of oral cancer, which need to be further explored. This article systematically introduces the mechanism of ferroptosis and its recent progress in oral cancer treatment to provide new mechanisms and methods for the clinical treatment of oral cancer. Current research shows that the mechanism of ferroptosis is mainly related to amino acid metabolism, Fe2+ metabolism, and lipid metabolism. Ferroptosis in oral cancer cells can reverse drug resistance in cancer cells and improve the activity of immune cells. New drugs, such as curcumin analogs and triptolide, can induce ferroptosis in oral cancer, and the development of nanomaterials has improved the utilization rate of drugs. Inhibiting the expression of the ferroptosis-related factors SLC7A11, NF-E2-related factor 2 (Nrf2), and ferritin heavy chain 1 (FTH1) can promote ferroptosis in oral cancer cells. It is a potential target for the clinical treatment of oral cancer, but its translation into clinical practice still needs further research.

Integration of cancer stemness and neoantigen load to predict responsiveness to anti-PD1/PDL1 therapy.

Background: Anti-programmed cell death 1/programmed cell death ligand 1 (PD1/PDL1) therapy is an important part of comprehensive cancer therapy. However, many patients suffer from non-response to therapy. Tumor neoantigen burden (TNB) and cancer stemness play essential roles in the responsiveness to therapy. Therefore, the identification of drug candidates for anti-PD1/PDL1 therapy remains an unmet need. Methods: Three anti-PD1/PDL1 therapy cohorts were obtained from GEO database and published literatures. Cancer immune characteristics were analyzed using CIBERSORTX, GSVA, and ESTIMATE. WGCNA was employed to identify the gene modules correlated with cancer TNB and stemness. A machine-learning method was used to construct the immunotherapy resistance score (TSIRS). Pharmacogenomic analysis was conducted to explore the potential alternative drugs for anti-PD1/PDL1 therapy resistant patients. CCK-8 assay, EdU assay and wound healing assay were used to validate the effect of the predicted drug on cancer cells. Results: The therapy response and non-response cancer groups have different microenvironment features. TSIRS was developed based on tumor neoantigen and stemness. TSIRS can effectively predict the outcomes of patients with anti-PD1/PDL1 therapy in training, validation and meta cohorts. Meanwhile, TSIRS can reflect the characteristics of tumor microenvironment during anti-PD1/PDL1 therapy. PF-4708671 is identified as a potential alternative drug for patients with resistance to anti-PD1/PDL1 therapy. It possesses significant inhibitive effect on the proliferation and migration of BGC-823 cells. Conclusion: TSIRS is an effective tool in the identification of candidate patients who will be benefit from anti-PD1/PDL1 therapy. Small molecule drug PF-4708671 has the potential to be used in anti-PD1/PDL1 therapy resistant patients.

COVID-19 and Gut Injury.

COVID-19 induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently a pandemic and it has led to more than 620 million patients with 6.56 million deaths globally. Males are more susceptible to COVID-19 infection and associated with a higher chance to develop severe COVID-19 than females. Aged people are at a high risk of COVID-19 infection, while young children have also increased cases. COVID-19 patients typically develop respiratory system pathologies, however symptoms in the gastrointestinal (GI) tract are also very common. Inflammatory cell recruitments and their secreted cytokines are found in the GI tract in COVID-19 patients. Microbiota changes are the key feature in COVID-19 patients with gut injury. Here, we review all current known mechanisms of COVID-19-induced gut injury, and the most acceptable one is that SARS-CoV-2 binds to angiotensin-converting enzyme 2 (ACE2) receptor on host cells in the GI tract. Interestingly, inflammatory bowel disease (IBD) is an inflammatory disorder, but the patients with IBD do not have the increased risk to develop COVID-19. There is currently no cure for COVID-19, but anti-viruses and monoclonal antibodies reduce viral load and shorten the recovery time of the disease. We summarize current therapeutics that target symptoms in the GI tract, including probiotics, ACE2 inhibitors and nutrients. These are promising therapeutic options for COVID-19-induced gut injury.

Extraordinarily Stable Aqueous Electrochromic Battery Based on Li4Ti5O12 and Hybrid Al3+/Zn2+ Electrolyte.

Aqueous electrochromic battery (ECB) is a multifunctional technology that shows great potential in various applications including energy-saving buildings and wearable batteries with visible energy levels. However, owing to the mismatch between traditional electrochromic materials and the electrolyte, aqueous ECBs generally exhibit poor cycling stability which bottlenecks their practical commercialization. Herein, we present an ultrastable electrochromic system composed of lithium titanate (Li4Ti5O12, LTO) electrode and Al3+/Zn2+ hybrid electrolyte. The fully compatible system exhibits excellent redox reaction reversibility, thus leading to extremely high cycling stabilities in optical contrast (12 500 cycles with unnoticeable degradation) and energy storage (4000 cycles with 82.6% retention of capacity), superior electrochromic performances including high optical contrast (∼74.73%) and fast responses (4.35 s/7.65 s for bleaching/coloring), as well as excellent discharge areal capacity of 151.94 mAh m-2. The extraordinary cycling stability can be attributed to the robust [TiO6] octahedral frameworks which remain chemically active even upon the gradual substitution of Li+ with Al3+ in LTO over multiple operation cycles. The high-performance electrochromic system demonstrated here not only makes the commercialization of low-cost, high-safety aqueous-based electrochromic devices possible but also provides potential design guidance for LTO-related materials used in aqueous-based energy storage devices.

Integrated Analysis Revealing the Senescence-Mediated Immune Heterogeneity of HCC and Construction of a Prognostic Model Based on Senescence-Related Non-Coding RNA Network.

Background: Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related mortality worldwide. Non-coding RNAs play an important role in HCC. This study aims to identify a senescence-related non-coding RNA network-based prognostic model for individualized therapies for HCC. Methods: HCC subtypes with senescence status were identified on the basis of the senescence-related genes. Immune status of the subtypes was analyzed by CIBERSORT and ESTIMATE algorithm. The differentially expressed mRNAs, microRNAs (miRNAs), and long non-coding RNAs (lncRNAs) were identified between the two HCC subtypes. A senescence-based competing endogenous RNA (ceRNA) co-expression network in HCC was constructed. On the basis of the ceRNA network, Lasso Cox regression was used to construct the senescence-related prognostic model (S score). The prognosis potential of the S score was evaluated in the training dataset and four external validation datasets. Finally, the potential of the prognostic model in predicting immune features and response to immunotherapy was evaluated. Results: The HCC samples were classified into senescence active and inactivate subtypes. The senescence active group showed an immune suppressive microenvironment compared to the senescence inactive group. A total of 2,902 mRNAs, 19 miRNAs, and 308 lncRNAs were identified between the two subtypes. A ceRNA network was constructed using these differentially expressed genes. On the basis of the ceRNA network, S score was constructed to predict the prognosis of patients with HCC. The S score was correlated with immune features and can predict response to immunotherapy of cancer. Conclusion: The present study analyzed the biological heterogeneity across senescence-related subtypes and constructed a senescence-related ceRNA-network-based prognostic model for predicting prognosis and immunotherapy responsiveness.

The whole transcriptome analysis and the circRNA-lncRNA network construction in arsenic trioxide-treated mice myocardium.

BACKGROUND/AIMS: Arsenic trioxide (ATO) is an effective anti-cancer drug. Nonetheless, it possesses cardiotoxic effects which limit its clinical application. The present study aims to elucidate the molecular basis of ATO-induced cardiotoxicity through using whole transcriptome analysis. METHODS: The whole transcriptome in ATO-treated mice myocardium was analyzed using RNA sequencing technique. These results were confirmed by real-time PCR. The lncRNA-mRNA and circRNA-mRNA co-expression networks were constructed. Finally, a circRNA-lncRNA co-regulated competing endogenous RNA (ceRNA) network was constructed. GO and KEGG pathway analyses were performed. The expression levels of Txnip and Spp1 in ATO-treated neonatal mouse cardiomyocytes were validated by real-time PCR. RESULTS: A total of 113 mRNAs, 159 lncRNAs, 35 miRNAs, and 94 circRNAs were differentially expressed in ATO-treated mice myocardium. A lncRNA-circRNA co-regulation network was constructed. Function annotation revealed that aberrantly expressed genes may be enriched in the 'Wnt signaling pathway', 'Hippo signaling pathway', 'Notch signaling pathway', etc. Finally, the expression levels of Txnip and Spp1 were validated in ATO-treated cardiomyocytes, which was in accordance with the RNA-sequencing results. CONCLUSION: ATO altered coding and noncoding RNA profiles in myocardium of mice. The ATO-related lncRNA-circRNA co-regulation network was constructed. Genes in the co-regulation network are likely to play important roles in the cardiotoxicity of ATO. This study provides new insights into the prevention and treatment of ATO-induced cardiotoxicity.

Loss of Hyaluronan and Proteoglycan Link Protein-1 Induces Tumorigenesis in Colorectal Cancer.

Colorectal cancer (CRC) is the third most common diagnosed cancer worldwide, but there are no effective cures for it. Hyaluronan and proteoglycan link protein-1 (HAPLN1) is a component of the extracellular matrix (ECM) proteins and involved in the tumor environment in the colon. Transforming growth factor (TGF)-ß is a key cytokine that regulates the deposition of ECM proteins in CRC. However, the role of HAPLN1 in TGF-ß contributions to CRC remains unknown. We found that the mRNA expression of HAPLN1 was decreased in tumors from CRC patients compared with healthy controls and normal tissue adjacent to the tumor using two existing microarray datasets. This was validated at the protein level by tissue array from CRC patients (n = 59). HAPLN1 protein levels were also reduced in human CRC epithelial cells after 24 h of TGF-ß stimulation, and its protein expression correlated with type I collagen alpha-1 (COL1A1) in CRC. Transfection of HAPLN1 overexpression plasmids into these cells increased protein levels but reduced COL1A1 protein, tumor growth, and cancer cell migration. TGF-ß stimulation increased Smad2/3, p-Smad2/3, Smad4, and E-adhesion proteins; however, HAPLN1 overexpression restored these proteins to baseline levels in CRC epithelial cells after TGF-ß stimulation. These findings suggest that HAPLN1 regulates the TGF-ß signaling pathway to control collagen deposition via the TGF-ß signaling pathway and mediates E-adhesion to control tumor growth. Thus, treatments that increase HAPLN1 levels may be a novel therapeutic option for CRC.

Observation and Suppression of Stacking Interface States in Sandwich-Structured Quantum Dot Light-Emitting Diodes.

Interfacial quality of functional layers plays an important role in the carrier transport of sandwich-structured devices. Although the suppression of interface states is crucial to the overall device performance, our understanding on their formation and annihilation mechanism via direct characterization is still quite limited. Here, we present a thorough study on the interface states present in the electron transport layer (ETL) of blue quantum dot (QD) light-emitting diodes (QLEDs). A ZnO/ZnMgO bilayer ETL is adopted to enhance the electron injection into blue QDs. By probing the ETL band structure with photoelectron spectroscopy, we discover that substantial band bending exists at the ZnO/ZnMgO interface, elucidating the presence of a high density of interface states which hinder electron transport. By inserting a ZnO@ZMO interlayer composed of mixed ZnO and ZnMgO nanoparticles, the band bending and thus the interface states are observed to reduce significantly. We attribute this to the hybrid surface properties of ZnO@ZMO, which can annihilate the surface states of both the ZnO and ZnMgO layers. The introduction of a bridging layer has led to ∼40% enhancement in the power efficiency of blue QLEDs and noticeable performance boosts in green and red QLEDs. The findings here demonstrate a direct observation of interface states via detailed band structure studies and outline a potential pathway for eliminating these states for better performances in sandwich-structured devices.

Efficiency Improvement of Quantum Dot Light-Emitting Diodes via Thermal Damage Suppression with HATCN.

With many advantages including superior color saturation and efficiency, quantum dot light-emitting diodes (QLEDs) are considered a promising candidate for the next-generation displays. Emission uniformity over the entire device area is a critical factor to the overall performance and reliability of QLEDs. In this work, we performed a thorough study on the origin of dark spots commonly observed in operating QLEDs and developed a strategy to eliminate these defects. Using advanced cross section fabrication and imaging techniques, we discovered the occurrence of voids in the organic hole transport layer and directly correlated them to the observed emission nonuniformity. Further investigations revealed that these voids are thermal damages induced during the subsequent thermal deposition of other functional layers and can act as leakage paths in the device. By inserting a thermo-tolerant 1,4,5,8,9,11-hexaazatriphenylene-hexacarbonitrile (HATCN) interlayer with an optimized thickness, the thermally induced dark spots can be completely suppressed, leading to a current efficiency increase by 18%. We further demonstrated that such a thermal passivation strategy can work universally for various types of organic layers with low thermal stability. Our findings here provide important guidance in enhancing the performances and reliability of QLEDs and also other sandwich-structured devices via the passivation of heat-sensitive layers.

Metal-Free Chemoselective Oxidation of 4-Methylquinolines into Quinoline-4-Carbaldehydes.

A convenient protocol for the synthesis of quinoline-4-carbaldehydes via chemoselective oxidation of 4-methylquinolines using hypervalent iodine(III) reagents as oxidant is described. This method highlights metal-free and mild reaction conditions, nice yield, good functional group tolerance, and high chemoselectivity.

Robust Ultralong Lead Halide Perovskite Microwire Lasers.

Hybrid organic-inorganic lead halide perovskite microwires are potential building blocks for realizing on-chip integrated optoelectronic devices. However, the length-controllable synthesis of one-dimensional hybrid perovskite microwires has been rarely reported, especially the ones with lengths in the millimeter scale. Herein, methylammonium lead bromide (MAPbBr3) and formamidinium lead bromide (FAPbBr3) micro and milliwires are demonstrated using single-crystal PbBr2 microwires synthesized via template-free solution-phase growth as the lattice framework. Following the PbBr2 template, the as-converted perovskite microwires possess controllable lengths ranging from tens to thousands of micrometers. In addition, Fabry-Perot (FP) lasing was realized in both MAPbBr3 and FAPbBr3 microwires, attesting to their excellent crystal quality and the efficient optical confinement of the natural cavity. These unique properties result in the first demonstration of FP perovskite microwire lasers with submillimeter lengths. More interestingly, the microwire lasers show excellent photostability under repetitive pulsed laser excitation for over 8 × 106 cycles. Such findings demonstrate that the solution-converted hybrid lead bromide microwires have excellent optoelectronic performances promising for practical applications, and the size controllability indicates that this novel fabrication process may be feasible for large-scale industrial production.

Sub-Nanometer Pt Clusters on Defective NiFe LDH Nanosheets as Trifunctional Electrocatalysts for Water Splitting and Rechargeable Hybrid Sodium-Air Batteries.

It is challenging to develop highly efficient and stable multifunctional electrocatalysts for improving the hydrogen evolution reaction (HER), the oxygen evolution reaction (OER), and the oxygen reduction reaction (ORR) for sustainable energy conversion and storage systems such as water-alkali electrolyzers (WAEs) and hybrid sodium-air batteries (HSABs). In this work, sub-nm Pt nanoclusters (NCs) on defective NiFe layered double hydroxide nanosheets (NixFe LDHs) are synthesized by a facile electrodeposition method. Due to the synergistic effect between Pt NCs and abundant atomic M(II) defects, along with hierarchical porous nanostructures, the Pt/NixFe LDHs catalysts exhibit superior trifunctional electrocatalytic activity and durability toward the HER/OER/ORR. A WAE fabricated with Pt/NixFe LDHs electrodes needs 1.47 V to reach a current density of 10 mA cm-2, much lower than that of the mixed 20% Pt/C and 20% Ir/C catalysts. An HSAB assembled by Pt/NixFe LDHs as a binder-free air cathode displays a high open-circuit voltage, a narrow overpotential gap, and remarkable rechargeability. This work provides a feasible strategy for constructing freestanding efficient trifunctional electrocatalysts for sustainable energy conversion and storage systems.

Photochemical Synthesis of 1,4-Dicarbonyl Bifluorene Compounds via Oxidative Radical Coupling Using TEMPO as the Oxygen Atom Donor.

A visible-light-induced metal-free synthesis of 1,4-dicarbonyl compounds from alkyne-containing aryl iodides via photochemical C-I bond cleavage, intramolecular cyclization, oxidation, and intermolecular radical coupling sequence is reported. TEMPO was employed as the oxygen atom donor in this transformation. This protocol provided a new strategy for the synthesis of 1,4-dicarbonyl bifluorene compounds.

Expression of Bex1 and NF-kBp65 in tongue squamous cell carcinoma and its significance / 口腔疾病防治

Objective @#To investigate the expression of brain expressed X-linked gene 1(Bex1) and nuclear factor-kBp65 (NF-kBp65) in tongue squamous cell carcinoma, and its significance.@*Methods@# Immunohistochemistry was used to detect the expression of Bex1 and NF-kBp65 in 60 tongue squamous cell carcinoma (TSCC) tissues and adjacent normal tissues, and the relationships between Bex1, NF-kBp65 and the clinicopathological features and prognosis of patients were analyzed.@*Results @#The positive expression rate of Bex1 in TSCC was 48.3% (29/60), which was significantly lower than that in adjacent normal tissues 88.3% (53/60) (x2=22.18, P < 0.01). The positive rate of Bex1 was negatively correlated with TNM stage, and the difference was statistically significant (P < 0.05). The positive rate of 63.3% (38/60) in TSCC was significantly higher than 20% (12/60) in adjacent normal tissues (x2=23.18, P < 0.01), the positive rate of NF-kBp65 was positively correlated with TNM stage, and the difference was statistically significant (P < 0.05). According to the Pearson correlation analysis results, the expression of Bex1 and NF-kBp65 in TSCC tissues was negatively correlated (r=-0.302, P=0.019). Kaplan-Meier survival curves showed that the survival rate of Bex1 positive patients was significantly higher than that of Bex1 negative patients.@*Conclusion @#In TSCC tissues, the low positive expression rate of Bex1 and the high positive expression rate of NF-kBp65 may promote tumor invasion and metastasis, and the negative expression of Bex1 may be related to the poor prognosis of patients.