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BACKGROUND: Pediatric patients undergoing liver transplantation are particularly susceptible to complications arising from intraoperative fluid management strategies. Conventional liberal fluid administration has been challenged due to its association with increased perioperative morbidity. This study aimed to assess the impact of intraoperative high-volume fluid therapy on pediatric patients who are undergoing living donor liver transplantation (LDLT). METHODS: Conducted at the Children's Hospital of Chongqing Medical University from March 2018 to April 2021, this retrospective study involved 90 pediatric patients divided into high-volume and non-high-volume fluid administration groups based on the 80th percentile of fluid administered. We collected the perioperative parameters and postoperative information of two groups. Multivariable logistic regression was utilized to assess the association between estimated blood loss (EBL) and high-volume FA. Kaplan-Meier survival analysis was used to compare patient survival after pediatric LDLT. RESULTS: Patients in the high-volume FA group received a higher EBL and longer length of stay than that in the non-high-volume FA group. Multivariate logistic regression analysis indicated that hours of maintenance fluids and fresh frozen plasma were significantly associated risk factors for the occurrence of EBL during pediatric LDLT. In addition, survival analysis showed no significant differences in one-year mortality between the groups. CONCLUSIONS: High-volume fluid administration during LDLT is linked with poorer intraoperative and postoperative outcomes among pediatric patients. These findings underscore the need for more conservative fluid management strategies in pediatric liver transplantations to enhance recovery and reduce complications.

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To investigate the effect of sevoflurane inhalation anesthesia on hemodynamics in children undergoing lower limb fracture surgery. Between January 2019 and December 2021, 187 kids at our hospital were randomly divided into two distinct categories: the experimental category (95 cases) and the control category (92 cases). Sevoflurane inhalation anesthesia was administered to the experimental cohort whereas Ketamine basic anesthesia was administered to the control cohort. Comparisons were made among the two categories' hemodynamic indices, anesthetic quality, and VAS ratings. When the eyelash reflex vanished, immediately after skin incision, as well as 5 min after skin incision, the SaO2, as well as MAP in the experimental group, were higher than those in the control category, while HR, SBP, as well as DBP were less than those in the control category. These variations were statistically noteworthy (P < .05). The onset of the experimental group's sensory blocks and the awakening of patients was faster than the control category, and the variations were of statistical importance (P < .05). At 24 hours, 48 hours, and 72 hours, the VAS score in the experimental category was substantially distinct from that in the control category (P < .05). In addition to lowering postoperative discomfort and stabilizing hemodynamics, sevoflurane inhalation anesthesia helps speed up the onset and recovery of anesthesia block in children having lower extremity fracture surgery.

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Aiming at the shortcomings of the traditional sparrow search algorithm (SSA) in path planning, such as its high time-consumption, long path length, it being easy to collide with static obstacles and its inability to avoid dynamic obstacles, this paper proposes a new improved SSA based on multi-strategies. Firstly, Cauchy reverse learning was used to initialize the sparrow population to avoid a premature convergence of the algorithm. Secondly, the sine-cosine algorithm was used to update the producers' position of the sparrow population and balance the global search and local exploration capabilities of the algorithm. Then, a Lévy flight strategy was used to update the scroungers' position to avoid the algorithm falling into the local optimum. Finally, the improved SSA and dynamic window approach (DWA) were combined to enhance the local obstacle avoidance ability of the algorithm. The proposed novel algorithm is named ISSA-DWA. Compared with the traditional SSA, the path length, path turning times and execution time planned by the ISSA-DWA are reduced by 13.42%, 63.02% and 51.35%, respectively, and the path smoothness is improved by 62.29%. The experimental results show that the ISSA-DWA proposed in this paper can not only solve the shortcomings of the SSA but can also plan a highly smooth path safely and efficiently in the complex dynamic obstacle environment.

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Prostate cancer is the most prevalent genitourinary malignant cancer in men worldwide. Patients with prostate cancer who progress to castration-resistant prostate cancer (CRPC) or metastatic CRPC have significantly poorer survival. Advanced prostate cancer is a clinical challenge due to the lack of effective treatment strategies. In the field of oncology, SGOL2 was an emerging and differentially expressed molecule, which enhanced the proliferation of cell populations in vitro in our studies. Mass spectrum and Co-IP validated the interaction of SGOL2 and RAB1A in a protein-protein manner. We further investigated the role of SGOL2 in the regulatory mechanism of RAB1A in prostate cancer cell lines. Furthermore, SGOL2 regulated RAB1A expression by inhibiting its ubiquitination. Rescue Experiments demonstrated that SGOL2 promoted prostate cancer cell proliferation and migration by upregulating RAB1A expression. Finally, we found that SGOL2 and RAB1A may regulate the tumor microenvironment (TME) in prostate cancer. In conclusion, our findings concluded that SGOL2 stabilized RAB1A expression to promote prostate cancer development. Both of them were of great importance in TME modulation.

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Multiple studies have indicated that long non-coding RNAs are aberrantly expressed in cancers and are pivotal in developing various tumors. No studies have investigated the expression and function of long non-coding antisense RNA PCNA-AS1 in esophageal squamous cell carcinoma (ESCC). In this study, the expression of PCNA-AS1 was identified by qRT-PCR. Cell function assays were used to explore the potential effect of PCNA-AS1 on ESCC progression. A prediction website was utilized to discover the relationships among PCNA-AS1, miR-2467-3p and proliferating cell nuclear antigen (PCNA). Dual luciferase reporter gene and RNA immunoprecipitation (RIP) assays were executed to verify the binding activity between PCNA-AS1, miR-2467-3p and PCNA. As a result, PCNA-AS1 was highly expressed in ESCC and was associated with patient prognosis. PCNA-AS1 overexpression strongly contributed to ESCC cell proliferation, invasion and migration. PCNA-AS1 and PCNA were positively correlated in ESCC. Bioinformatics analysis, RIP and luciferase reporter gene assays revealed that PCNA-AS1 could act as a competitive endogenous RNA to sponge miR-2467-3p, thus upregulating PCNA. In conclusion, the current outcome demonstrates that PCNA-AS1 may be a star molecule in the treatment of ESCC.

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OBJECTIVE: Abnormal expression of transforming acidic coiled-coil protein 3 (TACC3) has been reported in many types of human malignancies. However, the expression of TACC3 and its clinical significance have not been well characterized in lung carcinoma (LUAD). The aim of this study was to investigate possible associations between tumor expression of TACC3 and the clinicopathological characteristics and prognosis of LUAD patients. METHODS: The expression of TACC3 in LUAD patients was determined using the Oncomine, Gene Expression Profiling Interactive Analysis (GEPIA), UALCAN, and Cancer Genome Atlas (TCGA) databases. The expression of TACC3 in LUAD tissues was also determined by qRT-PCR. RESULTS: TACC3 was found to be significantly overexpressed in LUAD tumors compared with non-tumor tissue in the above public databases. Receiver operating characteristic (ROC) curve analysis indicated that TACC3 could have diagnostic value in LUAD patients. Kaplan-Meier analysis further indicated that high TACC3 expression in tumors was significantly associated with worse overall survival (OS) in LUAD patients. In addition, univariate and multivariate Cox regression analyses showed that high TACC3 expression was an independent factor for worse OS in LUAD patients. Finally, based on gene set enrichment analysis (GSEA 3.0), we identified several potential pathways related to TACC3 that were enriched in the high TACC3 expression phenotype. CONCLUSIONS: The present study provides evidence that TACC3 expression is upregulated in LUAD and may be an independent risk factor for worse prognosis in these patients.

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Objective: To investigate into the clinical factors associated with posttreatment recurrence and death patterns in patients with advanced esophageal cancer. Methods: Clinical information of patients with recurrence/metastasis and death after radical resection of esophageal cancer at our hospital between January 1, 2005, and December 31, 2015, were retrospectively collected and followed up. Postoperative recurrence-free survival time, postrelapse survival time, and overall survival time were compared among the metabolic-associated, organ failure-associated, and anastomotic recurrence-associated mortality groups. Results: Five hundred and ninety-five qualified patients were retrieved, including 456 males and 139 females, with an average age of 58 ± 7.56 years. There were 57 cases of TNM-1 stage, 131 cases of TNM-2 stage, 365 cases of TNM-3 stage, and 42 cases of TNM-4 stage. There were 547 cases of squamous cell cancer and 48 cases of nonsquamous cell cancer. There were significant differences in age (p < 0.01), tumor location (p < 0.01), and lymph node metastasis (p = 0.04), recurrence type (p < 0.01) by one-way ANOVA, and recurrence-free survival (p = 0.02) and postrecurrence survival (p < 0.01) by Kaplan-Meier survival curve analysis among the three main death causes. Conclusions: Age, tumor location, and lymph node metastasis were significantly different among metabolic-associated, organ failure-associated, and anastomotic recurrence-associated mortality of recurrent EC patients.

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ABSTRACTFood waste is an excellent organic matter for anaerobic fermentation. This study provided a cost-effective and highly efficient volatile fatty acid (VFA) production strategy by the addition of zero-valent iron (ZVI). Results showed that VFA concentration of 44.6 g/L was obtained with the optimized conditions of 200-mesh iron powder at a dosage of 20.0 g, fermentation time of 11 d, total solids (TS) of 10 wt.%, and fermentation temperature of 37 ℃. Further, the iron of different particle sizes (iron scraps, 200-mesh iron powder, and 800-mesh iron powder) had a differential influence on total organic carbon (TOC), total nitrogen (TN), and VFA concentrations. For the reactor containing 200-mesh iron powder, the conversion rate of organic compound into VFA increased with the increase of dosage, which reached 58.4% at the 40.0 g dosage. The mechanism revealed that the VFA production was enhanced by micro-electrolysis, which can rapidly inactivate bacteria and increase the conversion of macromolecular organics into micromolecular organics.

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BACKGROUND: Mirror-image pain (MIP), which develops from the healthy body region contralateral to the actual injured site, is a mysterious pain phenomenon accompanying many chronic pain conditions, such as complex regional pain syndrome (CRPS). However, the pathogenesis of MIP still remains largely unknown. The purpose of this study is to perform an expression profiling to identify genes related to MIP in an animal model of CRPS-I. METHODS: We established a rat chronic post-ischemic pain (CPIP) model to mimic human CRPS-I. RNA-sequencing (RNA-Seq), bioinformatics, qPCR, immunostaining, and animal behavioral assays were used to screen potential genes in the contralateral dorsal root ganglia (DRG) that may be involved in MIP. RESULTS: The CPIP model rats developed robust and persistent MIP in contralateral hind paws. Bilateral DRG neurons did not exhibit obvious neuronal damage. RNA-Seq of contralateral DRG from CPIP model rats identified a total 527 differentially expressed genes (DEGs) vs sham rats. The expression changes of several representative DEGs were further verified by qPCR. Bioinformatics analysis indicated that the immune system process, innate immune response, and cell adhesion were among the mostly enriched biological processes, which are important processes involved in pain sensitization, neuroinflammation, and chronic pain. We further identified DEGs potentially involved in pain mechanisms or enriched in small- to medium-sized sensory neurons or TRPV1-lineage nociceptors. By comparing with published datasets summarizing genes enriched in pain mechanisms, we sorted out a core set of genes which might contribute to nociception and the pain mechanism in MIP. CONCLUSION: We provided by far the first study to profile gene expression changes and pathway analysis of contralateral DRG for the studying of MIP mechanisms. This work may provide novel insights into understanding the mysterious mechanisms underlying MIP.

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Growing evidence has demonstrated that transforming acidic coiled-coil protein 3 (TACC3), a member of the TACC family, may be involved in regulating cell mitosis, transcription, and tumorigenesis. However, the role of TACC3 in kidney renal clear cell carcinoma (KIRC) remains unknown. In this study, multiple databases were used to determine the pattern of TACC3 in KIRC. We found that high TACC3 expression was associated with poor overall survival (OS) in stage I, II, IV and grade 3 KIRC patients. Univariate and multivariate Cox regression analyses showed that TACC3 was an independent risk factor for OS among KIRC patients. Moreover, TACC3 expression correlated with immune cell infiltration levels of B cells, T cells (CD8+, CD4+, follicular helper, regulatory and gamma delta), total and resting natural killer cells, total and activated dendritic cells, and resting mast cells. Furthermore, T cell exhaustion markers, such as PD1, CTLA4, LAG3 and TIM-3 were highly expressed in TACC3 overexpressing tissues. In addition, GSEA analysis revealed that the role of TACC3 in KIRC may be closely linked to immune-associated pathways. Therefore, our study reveals that TACC3 is a prognostic biomarker for OS among KIRC patients and may be associated with immune cell infiltration and T cell exhaustion.

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Liver hepatocellular carcinoma (LIHC) is one of the most lethal tumors worldwide, and while its detailed mechanism of occurrence remains unclear, an early diagnosis of LIHC could significantly improve the 5-years survival of LIHC patients. It is therefore imperative to explore novel molecular markers for the early diagnosis and to develop efficient therapies for LIHC patients. Currently, DEPDC1B has been reported to participate in the regulation of cell mitosis, transcription, and tumorigenesis. To explore the valuable diagnostic and prognostic markers for LIHC and further elucidate the mechanisms underlying DEPDC1B-related LIHC, numerous databases, such as Oncomine, Gene Expression Profiling Interactive Analysis (GEPIA), UALCAN, Kaplan-Meier plotter, and The Cancer Genome Atlas (TCGA) were employed to determine the association between the expression of DEPDC1B and prognosis in LIHC patients. Generally, the DEPDC1B mRNA level was highly expressed in LIHC tissues, compared with that in normal tissues (p < 0.01). High DEPDC1B expression was associated with poor overall survival (OS) in LIHC patients, especially in stage II, IV, and grade I, II, III patients (all p < 0.05). The univariate and multivariate Cox regression analysis showed that DEPDC1B was an independent risk factor for OS among LIHC patients (HR = 1.3, 95% CI: 1.08-1.6, p = 0.007). In addition, the protein expression of DEPDC1B was validated using Human Protein Atlas database. Furthermore, the expression of DEPDC1B was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR) assay using five pairs of matched LIHC tissues and their adjacent noncancerous tissues. The KEGG pathway analysis indicated that high expression of DEPDC1B may be associated with several signaling pathways, such as MAPK signaling, the regulation of actin cytoskeleton, p53 signaling, and the Wnt signaling pathways. Furthermore, high DEPDC1B expression may be significantly associated with various cancers. Conclusively, DEPDC1B may be an independent risk factor for OS among LIHC cancer patients and may be used as an early diagnostic marker in patients with LIHC.

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OBJECTIVE: The sedative effects of dexmedetomidine (Dex) are similar to natural sleep, with easy wakening following Dex administration, and Dex has minor effects on breathing, reducing emergence agitation in children. The aim of this study was to systematically evaluate the effects of Dex on recovery quality in children following general anaesthesia with sevoflurane, to aid clinical decision making. METHODS: Relevant randomized controlled trials published before August 2019 were searched and selected from databases. Two researchers independently screened the literature, extracted data, and assessed included studies for bias risk. Meta-analysis was performed using Stata 14.0 software. RESULTS: The study included 24 publications. Following general anaesthesia by sevoflurane, Dex was associated with reduced occurrence of emergence agitation (odds ratio [OR] 0.16, 95% confidence interval [CI] 0.11, 0.25) and nausea and vomiting (OR 0.40, 95% CI 0.24, 0.60), along with shortened eye-opening time (standardized mean difference [SMD] 0.72, 95% CI 0.41, 1.03), shortened extubation time (SMD 0.54, 95% CI 0.28, 0.81), and reduced duration of post-anaesthesia care unit (PACU) stay (SMD 0.29, 95% CI 0.08, 0.51) versus placebo. CONCLUSION: Dexmedetomidine has positive effects on recovery quality in children undergoing general anaesthesia with sevoflurane.

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In this study, Fe/Cu, Fe/Al/Cu, Fe/Cu/C and Fe/Al/Cu/C internal electrolysis systems (IESs) were constructed and used to treat methylene blue dye (MB) wastewater. The effects of filler mass ratio, filler dosage, solution pH, reaction time and reaction temperature on COD removal were discussed, while the kinetics, thermodynamics and mechanism of COD removal were also investigated. The results showed that when the COD removal rates were basically the same, the reaction times of Fe/Al/Cu, Fe/Cu/C and Fe/Al/Cu/C IESs were shorter, and the filler dosages were lower. For the four systems, the appropriate pH was around 5, while the suitable reaction temperature was in the range of 20-25 °C. The COD removals of these four IESs were generally greater than 90%. The COD removal processes of the four systems could be better described by the improved pseudo-second-kinetic model, and the liquid film diffusion was the rate-controlling step. Moreover, the COD removal was a spontaneous and endothermic process. MB was degraded into inorganic substances in four steps. In addition, the FTIR characterization of the fillers before and after reaction suggests the four IESs have good stability.

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Long non-coding RNA taurine up-regulated gene 1 (TUG1) emerges as new players in gene regulation in several cancers; however, its mechanism of action in non-small cell lung cancer (NSCLC) has not been well-studied. Herein, we determined expression pattern of TUG1 in NSCLC and further identified its effect on the chemosensitivity of NSCLC. Low expression of TUG1 was found in NSCLC tissues obtained from non-responders to platinum-based chemotherapy and reflected poor overall survival. TUG1 overexpression was shown to inhibit cell proliferation, migration, invasion, but facilitate apoptosis and autophagy in NSCLC cells resistant to cisplatin (DDP). Smaller size of tumor xenografts of DDP resistant NSCLC cells in the presence of TUG1 demonstrated enhancement of chemosensitivity by TUG1 in vivo. High expression of miR-221 and low expression of PTEN were determined in cancer tissues obtained from non-responders to platinum-based chemotherapy and reflected poor overall survival. TUG1 inhibited miR-221 that targeted PTEN, as evidenced by an elevated expression of PTEN in the presence of miR-221 or the absence of TUG1. Our present study reveals a model of enhancement of chemosensitivity that consists of TUG1, miR-221 and PTEN. Modulation of their levels may offer a new approach for improving anti-tumor efficacy for chemotherapeutic agents in NSCLC.

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We have prepared core/shell structured hollow Fe-Pd@C nanomaterials derived from Fe-metal organic frameworks which were synthesized via cheap, fast and simple mechanochemical technique. The obtained Fe-Pd@C can steadily and continuously release Fe2+ from the galvanic corrosion of Fe0 anode to trigger H2O2 decomposition into hydroxyl radicals and cause fast (10 min) and efficient (mineralization rate 95%) degradation of phenol. The presence of low level of Pd NPs in Fe-Pd@C (mass ratio of the raw material: Fe/Pd = 100:1) facilitated fast Fe3+/Fe2+ redox cycle and thus improved the catalytic performance and pH endurance of the Fe-Pd@C. After recycled four times, Fe-Pd@C remained high catalytic performance and released low level of iron ions (2.5 mg L-1), which reduced the production of iron sludge after usage. In contrast to zero-valent iron (ZVI) and commercial physically mixed Fe/C materials, the core/shell structure of Fe-Pd@C ensured efficient electron transferring from Fe0 to carbon cathode and targets, and prevented the precipitation of iron ions on Fe0 surface, avoiding the deactivation of Fe0 and termination of Fe-C internal micro-electrolysis (IME) and extending their service life. The reactive species quenching experiments and ESR characterization proved the synergistic effect of electrons and hydroxyl free radicals on degradation of phenol. The carbon-centered DMPO radical detected in reaction solution can be regarded as a proof for the strengthened oxidation ability of the combined IME and Fenton reaction.

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Lung cancer remains the leading cause of cancer associated deaths worldwide. Recent efforts have been focused on combinational and nanoparticulate therapies that can efficiently deliver multiple therapeutics. Herein, we reported cetuximab (CET) functionalized, paclitaxel (PTX) and 5-Demethylnobiletin (DMN) co-loaded nanostructured lipid carriers (NLCs) (CET-PTX/DMN-NLCs). The morphology, particle size, zeta potential, stability and drug release were tested. Cellular uptake, cell viability, synergistic effects and in vivo anti-tumor effects were evaluated on human lung adenocarcinoma cells (A549 cells), human embryonic lung cells (MRC-5 cells) and A549 paclitaxel-resistant cells bearing mice models. NLCs had sizes of around 130 nm and zeta potentials of +20-30 mV. The release of drugs from NLCs was relatively fast at the first 12 h and then became slow until completion of sustained release behavior. Cells uptake of CET-PTX/DMN-NLCs (65.8%) was remarkably higher than that of PTX/DMN-NLCs (35.5%) in A549 cells. The combination treatment with PTX and DMN synergistically decreases the viability of cells than the single PTX-NLCs and DMN-NLCs. CET-PTX/DMN-NLCs exhibited the most remarkable in vivo tumor inhibition efficiency, which suspended the tumor growth from 1010.23 to 211.18 mm3 at the end of the study. The highest tumor accumulation amount and low toxicity made CET-PTX/DMN-NLCs a promising system for the synergistic combination therapy of lung cancer.

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Endothelin-1 (ET-1) is a potent endogenous vasoconstrictor that has been widely known as a pain mediator involved in various pain states. Evidence indicates that ET-1 sensitizes transient receptor potential cation channel, subfamily A, member 1 (TRPA1) in vivo. But the molecular mechanisms still remain unknown. We aim to explore whether ET-1 sensitizes TRPA1 in primary sensory neurons and the molecular mechanisms. Ca2+ imaging, immunostaining, electrophysiology, animal behavioral assay combined with pharmacological experiments were performed. ET-1 sensitized TRPA1-mediated Ca2+ responses in human embryonic kidney (HEK)293 cells as well as in cultured native mouse dorsal root ganglion (DRG) neurons. ET-1 also sensitized TRPA1 channel currents. ET-1 sensitized TRPA1 activated by endogenous agonist H2O2. ETA receptor (ETAR) colocalized with TRPA1 in DRG neurons. ET-1-induced TRPA1 sensitization in vivo was mediated via ETAR and protein kinase A (PKA) pathway in HEK293 cells and DRG neurons. Pharmacological blocking of ETAR, PKA, and TRPA1 significantly attenuated ET-1-induced mechanical hyperalgesia in mice. Our results suggest that TRPA1 acts as a molecular target for ET-1, and sensitization of TRPA1 through ETAR-PKA pathway contributes to ET-1-induced mechanical hyperalgesia. Pharmacological targeting of TRPA1 and ETAR-PKA pathway may provide effective strategies to alleviate pain conditions associated with ET-1.

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Our aim was to study the regulatory molecule networks involved in the epithelial-to-mesenchymal transition and thus promoting the early onset of metastasis in triple-negative breast cancer (TNBC). Forty pairs of human TNBC and their adjacent normal breast tissues were analyzed by real-time PCR and immunochemistry to demonstrate the correlation between the miR-205 expression and clinicopathological characteristics. In vitro, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, cell migration, and invasion assay were used to detect the cell growth and invasive ability of TNBC cells after upregulation or downregulation of miR-205 expression. Luciferase reporter assay was used to confirm the potential target directly influenced by miR-205. Our results showed that miR-205 abnormal expression may be involved and associated with the biological traits of TNBC. Ectopic expression of miR-205 not only inhibited cell growth, but also suppressed migration and invasion of mesenchymal-like TNBC cells. In addition, we found that overexpression of miR-205 significantly suppressed HMGB1 by binding its 3'-untranslated region, and that miR-205 was inversely correlated with the expression of HMGB1 and RAGE in cell lines and clinical samples. Our study illustrated that miR-205 was a tumor suppressor in TNBC, which attenuated the viability and the acquisition of the epithelial-to-mesenchymal transition phenotype TNBC cells at least partially exerted through targeting of HMGB1-RAGE signaling pathway.

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@#肿瘤的生长需要血管的生成，不同于正常的血管，异常的肿瘤血管通过改变肿瘤微环境来抑制机体的免疫功能，从而 使肿瘤发生免疫逃逸。抗血管生成治疗可以使肿瘤血管正常化，进而改善机体的免疫功能。免疫检查点抑制剂通过改变肿瘤微 环境，不仅可以提高机体的免疫功能，同时也可以促进肿瘤血管的正常化。本文综述了抗血管生成治疗联合免疫检查点抑制剂 治疗恶性肿瘤的理论依据以及相关的临床数据，为恶性肿瘤的治疗提供更多的治疗策略。

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A murine monoclonal antibody (MAb-1) specific for GM3 has been generated by immunizing ß3Gn-T5 knockout mice with purified GM3 ganglioside. The binding specificity of MAb-1 (IgG3 subclass) was established by an enzyme-linked immunosorbent assay (ELISA) and FACS and the antibody showed high binding specificity with GM3. Cell viability assay showed that MAb-1 significantly suppressed cell growth. Immunohistochemistry analysis revealed that MAb-1 was strongly expressed in human ovarian cancer tissues, whereas it was hardly expressed in normal tissues. Finally, antibody-dependent cellular cytotoxicity (ADCC) activities were determined by measuring lactate dehydrogenase (LDH) releasing assay and the results showed high ADCC activities in two representative ovarian cancer cell lines (OVHM and ID8). All of these data indicate that MAb-1 may be potentially used as a therapeutic antibody against ovarian cancers in clinical trials.

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