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Long non-coding RNAs (lncRNAs), a group of non-coding RNAs with lengths exceeding 200 nucleotides, play a crucial role in the human transcriptome, particularly in various types of cancers, where they are pivotal in regulating the tumor immune microenvironment and tumor cell immune evasion.However, there is currently a lack of systematic literature review. Myeloid-derived suppressor cells (MDSCs), a subset of myeloid cells with immunosuppressive functions, play a significant role in cancer by directly and indirectly suppressing T cell activity, promoting the expansion of regulatory T cells, modulating the tumor microenvironment, and facilitating tumor metastasis. This review emphasizes the importance of in-depth investigation into the regulatory mechanisms of MDSCs for the discovery of effective tumor therapeutic targets and the development of novel treatment strategies. With further understanding and research into the relationship between lncRNAs and MDSCs, it is anticipated that more targets and new therapeutic approaches will be identified for cancer treatment, thereby improving clinical outcomes for patients. [ABSTRACT FROM AUTHOR]

Objective: To compare the changes in serum renin angiotensin aldosterone (RAAS) system indicators and serum high mobility group protein 1 (HMGB1), soluble myeloid cell trigger receptor-1 (sTREM-1), and Toll like receptor-4 (TLR4) levels in patients with sepsis complicated by acute kidney injury (AKI) after intermittent hemodialysis (IHD) and continuous blood purification (CBP) treatment. Methods: 107 patients with sepsis combine with AKI admitted to our hospital from January 2019 to June 2023 were selected. Patients were divided into intermittent group (n=53, receiving IHD treatment) and continuous group (n=54, receiving CBP treatment) according to the random number table method. The RAAS system indexes, serum sTREM-1, HMGB1, TLR4, renal function and immune function indexes were compared between two groups. Results: After treatment, the renin activity (PRA), aldosterone (ALD), angiotensin I (AngI), sTREM-1, HMGB1, TLR4, urea nitrogen (BUN) and serum creatinine (Scr) in two groups decreased, and those in continuous group were lower than those in intermittent group (P<0.05). After treatment, CD8 decreased in both groups, and continuous group was lower than than in intermittent group. CD3, CD4, CD4/CD8" increased, and continuous group were higher than those in intermittent group (P<0.05). Conclusion: Compared with IHD treatment, CBP treatment of sepsis combine with AKI, which can further improve renal function, improve immune function, regulate RAAS system indexes and serum sTREM-1, HMGB1, TLR4 levels. [ABSTRACT FROM AUTHOR]

Objective: To explore the relationship between the therapeutic effect of Fu Yuan Sheng Bai Fang (FYSBF) on acute myeloid leukemia (AML) and the JAK/STAT signaling pathway and its mechanism. Methods: AML HL-60 cells were divided into control group, FYSBF group, IL-6 group (IL-6 is the activator of JAK/STAT signaling pathway) and FYSBF+IL-6 group. HL-60 cells in control group were cultured in normal RPMI 1640 medium, HL-60 cells in FYSBF group were cultured in medium which was added with a final concentration of 200 μg/m L FYSBF, and HL-60 cells in IL-6 group were cultured in medium which was added with a final concentration of 100 ng/mL IL-6. HL-60 cells in FYSBF+IL-6 group were cultured in medium which were added with final concentration of 200 μg/m L FYSBF and 100 ng/mL IL-6. The cell proliferation was detected by CCK-8 assay and clonal formation assay, cell cycle distribution and apoptosis were detected by flow cytometry, cell invasion and migration were detected by Transwell assay, and protein expression levels were analyzed by Western blot assay. Results: Compared with the control group, the relative vitality, number of clones, number of migration and invasion cells and proportion of S-phase cells in FYSBF group were decreased (P＜0.05), and the protein expressions of CDK2, cyclin E, N-cadherin and Vimentin were decreased (P＜0.05), the phosphorylation levels of JAK2 and STAT3proteins were decreased (P＜0.05), the cells proportion of G0/G1 phase and apoptosis rate were increased (P＜0.05), and the protein expression of p21 and E-cadherin were increased (P＜0.05) . Compared with the control group, the relative vitality, number of clones, number of migration and invasion cells and proportion of S-phase cells in IL-6 group were increased (P＜0.05), and the protein expressions of CDK2, cyclin E, N-cadherin and Vimentin were increased (P＜0.05), the phosphorylation levels of JAK2 and STAT3proteins were increased (P＜0.05), the cells proportion of G0/G1 phase and apoptosis rate were decreased (P＜0.05), and the protein expression of p21 and E-cadherin were decreased (P＜0.05) . Compared with the IL-6 group, the relative vitality, number of clones, number of migration and invasion cells and proportion of S-phase cells in FYSBF+IL-6 group were decreased (P＜0.05), and the protein expressions of CDK2, cyclin E, N-cadherin and Vimentin were decreased (P＜0.05), the phosphorylation levels of JAK2 and STAT3proteins were decreased (P＜0.05), the cells proportion of G0/G1 phase and apoptosis rate were increased (P＜0.05), and the protein expression of p21 and E-cadherin were increased (P＜0.05) . Conclusion: FYSBF can inhibit the proliferation, migration, invasion and epithelial-mesenchymal transformation of acute myeloid leukemia cells, and promote cell apoptosis and cell cycle arrest, which may be related to inhibiting the activation of JAK2/STAT3 pathway. [ABSTRACT FROM AUTHOR]

Objective Periodontitis and Alzheimer’s disease are prevalent among the elderly, with an incidence that increases with age. To investigate the potential common pathogenic factors between the two diseases and provide a theoretical basis for the early diagnosis of Alzheimer’s disease, the study analyzed the pathogenic risk correlation between periodontitis and Alzheimer’s disease using single-cell transcriptomics data and Bulk RNA-seq sequencing data. Methods Single-cell data for PD (GSE164241) and AD (GSE157827) were downloaded from the Gene Expression Omnibus (GEO) database, including samples from 3 patients and 3 controls for each condition. The single-cell data were subjected to quality control, data integration, dimensionality reduction clustering, cell type annotation, and differential gene expression identification. Shared differentially expressed genes between the two diseases were identified by comparing the gene expression profiles. Enrichment analysis of these shared genes was conducted, followed by the construction of a protein-protein interaction (PPI) network to understand the interactions between proteins. Bulk RNA-seq microarray expression matrices and sample information for PD (GSE16134) and AD (GSE63060) were downloaded from the GEO database to validate the expression levels of core genes in the PPI network from the single-cell data and to assess the correlation between genes and diseases. Results Comparative analysis of sample data from periodontitis and Alzheimer’s disease revealed CD163+ myeloid cells as a common immune cell type in both conditions. In periodontitis-derived myeloid cells, 1934 downregulated differentially expressed genes were found in the disease group compared to the control group, while in Alzheimer’s disease-derived myeloid cells, 232 downregulated genes were identified, with an intersection of 49 shared downregulated genes. Enrichment analysis of these genes primarily highlighted myeloid cell and complement system-related responses. Further analysis showed that the expression of STAB1 gene in the complement system was significantly negatively correlated with both periodontitis and Alzheimer’s disease. Conclusion Myeloid cells are a common immune cell type in both periodontitis and Alzheimer’s disease. STAB1 acts as a downstream target of complement pathway closely related to both diseases and shows a significant negative correlation with disease onset. This suggests that the detection of STAB1 gene expression levels in periodontitis patients could serve as potential targets for the early diagnosis and treatment of Alzheimer’s disease.

The importance of amino acid metabolism has been gradually recognized, and the relationship between arginine metabolism and tumors has become a hot topic. Arginine is a conditionally essential amino acid, which is closely related to the occurrence, growth and metastasis of tumors. The formation of an immunosuppressive microenvironment, and the phenotypic changes, maturation and functional status of myeloid immune cells are also inseparable from arginine metabolism. This article mainly elucidates how arginine metabolism affects tumors and the role of arginine in anti-tumor immunity, summarizes the main myeloid immune cells in the tumor microenvironment, and briefly summarizes the tumor treatment strategies that target the arginine metabolism pathway. [ABSTRACT FROM AUTHOR]

Objective: To establish a mouse model of breast cancer lung metastasis with miR-155 knockout (miR155-/-) mice, and to compare the difference of peripheral blood immune cell typing between miR155-/- mice and C57BL/6J wide-type (WT) mice. Methods: Bioinformatics analysis was used to explore the expression level of miR-155 in breast cancer tissues and peripheral serum, and its relationship with prognosis. Mouse model of lung metastasis of breast cancer was established by tail vein injection; peripheral blood was collected for flow cytometry, and the immune cell typing was analyzed; the lung tissues were collected for immunohisto-chemical detection to observe the tumor metastasis. Results: Percentage of T lymphocytes and monocytes in peripheral blood of miR155-/- mice was significantly decreased compared with WT mice (P<0.05), percentage of myeloid inhibitory cells (MDSCs) was increased significantly (P<0.05), in which the proportion of monocyte subsets (M-MDSC) was significantly decreased (P<0.05), while the proportion of granulocyte subsets (G-MDSC) was significantly increased (P<0.05). In lung metastasis model of breast cancer, percentage of T lymphocytes in peripheral blood of miR155-/- mice was significantly higher compared with WT mice, while percentage of NK cells was decreased significantly (P<0.05), percentage of neutrophil was significantly decreased (P<0.001), proportion of Th cells in T lymphocytes was significantly decreased (P<0.05), proportion of M-MDSCs was significantly decreased (P< 0.01), while proportion of G-MDSCs was significantly increased (P<0.01). Conclusion: Deletion of miR-155 gene leads to significant differences in peripheral immune cell typing, making mice more susceptible to lung metastasis of breast cancer. [ABSTRACT FROM AUTHOR]

BACKGROUND: Intervertebral disc degeneration is the basis of spinal degenerative diseases; however, there is no effective treatment. OBJECTIVE: To investigate whether sinomenine can inhibit interleukin-1β-induced apoptosis in nucleus pulposus cells and its molecular mechanism. METHODS: Rat nucleus pulposus cells were cultured in vitro by trypsin combined with type II collagenase digestion, and the cell growth curve was plotted. An appropriate sinomenine concentration was determined using the cell counting kit-8 kit. Nucleus pulposus cells were divided into control group, sinomenine group, interleukin-1β group, sinomenine+interleukin-1β group, zinc protoporphyrin group, zinc protoporphyrin+sinomenine group, zinc protoporphyrin+interleukin-1β group, and sinomenine+zinc protoporphyrin+interleukin-1β group. Proliferative activity, reactive oxygen species content, apoptosis rate, and heme oxygenase-1 expression in nucleus pulposus cells were detected. RESULTS AND CONCLUSION: The rat nucleus pulposus cells cultured in vitro were polygonal, triangular, and short wedge-shaped, and the cell growth showed an “S” curve. The cells grew slowly in the first 3 days of culture, rapidly in 4-6 days, and slowly again in 7-8 days. The cells then entered the “platform stage” where the number of cells no longer increased. The proliferative activity of myeloid cells showed no significant changes when the concentration of sinomenine was ≤ 80 μmol/L (P > 0.05). Interleukin-1β significantly reduced the proliferative activity of nucleus pulposus cells, increased the content of reactive oxygen species and led to apoptosis (P < 0.01). Sinomenine intervention not only promoted heme oxygenase-1 expression (P < 0.05) but also inhibited interleukin-1βinduced decrease in proliferative activity and increase in reactive oxygen species content and apoptosis rate in nucleus pulposus cells (P < 0.05). These effects could be reversed by zinc protoporphyrin (P < 0.01). [ABSTRACT FROM AUTHOR]

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective.To investigate the impacts of chlorprothixene on autophagy and apoptosis in human acute myeloid leukemia (AML) cells by regulating the protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway. Methods.Two cell lines, SKNO-1 and MOLM-13, were used as the research objects, and they were treated with (0, 20, 40, 60) μmol/L chlorprothixene for (6, 12, 24) h, respectively, CCK-8 was performed to detect cell proliferation.Experiments were divided into control group (normal culture), SC79 group (5 mg/L SC79 treated cells for 2 h),chlorprothixene group (40 μmol/L chloroprotixol treated cells for 12 h), chlorprothixene + SC79 group (40 μmol/L chlorprothixene was added to the cells for 12 h on the basis of the group), monodansylcadaverine (MDC) staining was performed to measure the occurrence of autophagy,flow cytometry was performed to measure cell apoptosis rate,Western blot was performed to measure autophagy-related protein SQSTM1/ p62, microtubule-related protein 1 light chain 3B (LC3B), apoptosis-related protein poly (ADP-ribosyltransferase) (PARP), aspartate-specific cysteine protease 3 (caspase3), activated caspase3 (cleaved caspase3) and Akt/mTOR signaling pathway related proteins Akt, phosphorylated (p)-Akt, mTOR and p-mTOR. Results.In SKNO-1 and MOLM-13 cells, at (6, 12, 24) h, compared with 0 μmol/L chlorprothixene, (20, 40, 60) μmol/L chlorprothixene treatment increased the inhibition rate of cell proliferation (P < 0.05),at the same time point, as the concentration of chlorprothixene increased, the inhibition rate of cell proliferation increased, and 40 μmol/L chlorprothixene treatment for 12 h was used for the next study.In SKNO-1 and MOLM-13 cells, compared with the control group, the apoptosis rate, autophagosome positive rate, LC3B, PARP, cleaved caspase3/caspase3 protein expression levels in SC79 group decreased (P < 0.05), the SQSTM1/p62, p-Akt/Akt and p-mTOR/mTOR protein expression levels increased (P < 0.05),the chlorprothixene group showed the opposite trends (P < 0.05),after adding chlorprothix ene on the basis of SC79 group, the apoptosis rate, autophagosome positive rate, LC3B, PARP, cleaved caspase3/ caspase3 protein expression levels decreased than chlorprothixene group (P < 0.05), the protein expression levels of SQSTM1/p62, p-Akt/Akt and p-mTOR/mTOR increased (P < 0.05). Conclusion.Chlorprothixene can inhibit the Akt/mTOR pathway and promote autophagy and apoptosis in human AML cells. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

AIM: To explore the effect of Yixinshu (YXS) tablets on acute myocardial infarction (MI) in mice and its related mechanism. METHODS: The potential targets of YXS were explored by combining TCMSP and Metascape for bioinformatics analysis. Sixty male C57BL/6J mice were randomly divided into 3 groups: sham operation group (sham group), model group (MI group), and Yixinshu tablet pretreatment group (YXS+MI group), with 20 mice in each group. The mice in YXS+MI group were given YXS (60 mg·kg-1 ·d-1 ) intragastric administration for 14 d, while those in sham group and MI group were given the same volume of normal saline. The MI model was established by ligation of the left ante⁃ rior descending coronary artery. The cardiac function was detected by ultrasonic Doppler 1 d after operation. Myocardial infarction size was detected by TTC staining. The infiltration of inflammatory cells at the infarct myocardium was analyzed by HE staining and CD45 immunohistochemistry. Myocardial ultrastructures and mitochondrial damage were observed by transmission electron microscopy. TUNEL staining was used to detect the apoptotic cells. Western blot were used to detect the levels of apoptosis-related proteins Bax and Bcl2, and flow cytometry was used to detect the infiltration of myeloid in⁃ flammatory cells. RESULTS: Compared with sham group, the left ventricular systolic function of the mice in MI group was impaired, with significant decreases in ejection fraction (EF) and shortened fraction (FS) (P<0. 05). In addition, the inflammatory cell infiltration in myocardial tissue increased, myocardial ultrastructure was damaged, the proportion of apoptotic cells significantly increased (P<0. 01), Bax protein level significantly increased (P<0. 01), and Bcl2 protein level significantly decreased (P<0. 01). Flow cytometry results showed a significant increase in the infiltration of myeloid inflammatory cells (P<0. 01). Compared with MI group, the mice in YXS+MI group showed significant increases in EF and FS (P<0. 05). Meanwhile, the infiltration of inflammatory cells in myocardial tissues was reduced, and the damage to myocardial ultrastructures was alleviated, the proportion of apoptotic cells significantly decreased (P<0. 01), with a de⁃ crease in Bax protein expression (P<0. 05), an increase in Bcl2 protein expression (P<0. 01) and a reduction of myeloid inflammatory cell infiltration (P<0. 05). CONCLUSION: Pretreatment with YXS alleviates myocardial injury after acute MI in mice, reduces cardiomyocyte apoptosis, and decreases the infiltration of myeloid inflammatory cells. [ABSTRACT FROM AUTHOR]

BACKGROUND: Knee osteoarthritis (KOA) is a common chronic inflammatory disease that causes damage to joint cartilage and surrounding tissues. Immune cells play an important role in the immune-inflammatory response in knee osteoarthritis, but the specific mechanisms involved are still not fully understood. OBJECTIVE: To evaluate the potential causal relationship between 731 immune cell phenotypes and the risk of knee osteoarthritis using Mendelian randomization. METHODS: Summary statistics of genome-wide association studies (GWAS) for 731 immune cell phenotypes (from GCST0001391 to GCST0002121) obtained from the GWAS catalog and GWAS data for knee osteoarthritis from the IEUGWAS database (ebi-a-GCST007090) were used. Inverse variance-weighted method, MR-Egger regression, weighted median method, weighted mode method, and simple mode method were employed to investigate the causal relationship between immune cells and knee osteoarthritis. Sensitivity analyses were conducted to assess the reliability of the Mendelian randomization results. Reverse Mendelian randomization analysis was also performed using the same methods. RESULTS AND CONCLUSION: The forward MR analysis indicated significant causal relationships (FDR < 0.20) between knee osteoarthritis and four immune cell phenotypes, namely CD27 on CD24+CD27+ in B cells (OR=1.026, P=0.000 26, Pfdr=0.18), CD33 on CD33dim HLA DR- in myeloid cells (OR=1.014, P=0.000 50, Pfdr=0.18), and CD45RA+CD28-CD8br %CD8br in Treg cells (OR=1.001, P=0.000 78, Pfdr=0.18), and PDL-1 on monocytes in mononuclear cells (OR=0.952, P=0.000 98, Pfdr=0.18). These immune cell phenotypes showed direct positive or negative causal associations with the risk of knee osteoarthritis. Reverse Mendelian randomization analysis revealed no significant causal relationships (FDR < 0.20) between knee osteoarthritis as exposure and any of the 731 immune cell phenotypes. The results of sensitivity analysis show that the P-values of the Cochran’s Q test and the MR-Egger regression method for bidirectional Mendelian randomization were both greater than 0.05, indicating that there is no significant heterogeneity and pleiotropy in the causal effect analysis between immune cell phenotypes and knee osteoarthritis. To conclude, there may be four potential causal relationships between immune cell phenotypes, such as CD27 on CD24+CD27+ cells, CD33 on CD33dim HLA DR- cells, CD45RA+CD28-CD8br %CD8br cells, and PDL-1 on monocytes, and knee osteoarthritis. These findings provide valuable clues for studying the biological mechanisms of knee osteoarthritis and exploring early prevention and treatment strategies. They also offer new directions for the development of intervention drugs. [ABSTRACT FROM AUTHOR]

BACKGROUND: To obtain a large number of high purity trophoblast-free, animal-derived natural killer (NK) cells from deep cryopreserved cord blood for better experimental studies on tumor killing by NK cells, a safe and efficient method for expanding and culturing NK cells in vitro was obtained by using NK expansion culture kits and serum substitutes. OBJECTIVE: To establish a technical system for the expansion of NK cells from frozen cord blood using pure cytokines, and demonstrate their tumor-killing ability in vitro. METHODS: The frozen cord blood stored in liquid nitrogen was thawed to optimize the recovery system. The individual nucleated cells were collected by Ficoll density gradient centrifugation and inoculated in pre-plated T175 culture flasks. Cells were cultured using the cytokine + serum replacement method for 21 days and counted. The ratio of CD3- CD56+ in cells was detected by flow cytometry. The data obtained were compared with the data of K562 trophoblast cells + fetal bovine serum culture method. Meanwhile, myeloid leukemia cells K562 were used as target cells, and CCK-8 kit was used to perform different potent target ratios of NK cells to kill K562 cells. Later, simulated storage transport experiments were performed for 12 hours. The changes in the ratio of CD3- CD56+ were detected by flow cytometry and the apoptosis ratio was determined using Annexin V/PI double-staining method. RESULTS AND CONCLUSION: (1) The cells were expanded and cultured for 14 days using K562 trophoblast cells + fetal bovine serum, and the cells expanded (51.47±4.28) fold. After 21 days of expansion culture using cytokine + serum substitute method, the number of cells was more than 5×109 ; the cells expanded (328.32±116.36) times; the cell expansion ploidy was significantly higher; the CD3- CD56+ purity ratio obtained by both methods was above 80%; no significant difference was seen. (2) The killing effect of NK cells cultured by pure cytokine method on K562 cells (effective target ratio=10:1) was more than 80%. (3) The ratio of CD3- CD56+ did not change significantly during the 12-hour simulated storage experiment until the 12 hours, when the apoptosis rate of NK cells was < 7%. (4) The results showed that the optimized recovery system and pure factor expansion method can efficiently culture high-purity NK cells with the ability to effectively kill K562 tumor cells, and still have good cell purity and low apoptosis rate after 12-hour storage and transportation. [ABSTRACT FROM AUTHOR]

Objective: This study aims to investigate the influence of triggering receptor expressed on myeloid cells 1 (TREM1) expression on the mitochondrial dynamics and apoptosis of chondrocytes in order to propose a novel direction for the treatment of osteoarthritis in the future. Methods: Murine chondrocyte ATDC5 cells were stimulated with interleukin-1β (IL-1β) to mimic osteoarthritis-like chondrocyte inflammation, and interleukin-6 (IL-6) expression was detected by qPCR to validate the inflammatory chondrocyte model. The expression of the target gene TREM1 was also detected by qPCR. To observe the effect of TREM1 inhibition on inflammatory chondrocytes, the cells were divided into the control group, IL-1β group and IL-1β+LR12 (TREM1 inhibitor) group. Mito-Tracker staining and TUNEL staining were used to observe the mitochondrial dynamics and apoptosis of the cells. The effects of TREM1 overexpression on normal ATDC5 chondrocytes were then investigated. The cells were divided into the vector group, TREM1 overexpression group, and TREM1 overexpression+LR12 group. Mito-Tracker staining and TUNEL staining were used to detect mitochondrial dynamics and apoptosis in all three groups. In addition, PCR Array was used to detect the effects of TREM1 overexpression on chondrocyte metabolism. Results: Compared with the control group, the expression of IL-6 was increased in the IL-1β group, indicating successful establishment of inflammatory chondrocytes. TREM1 expression was also elevated in IL-1β-treated chondrocytes. However, treatment with an inhibitor of TREM1 (LR12) effectively inhibited the expression of TREM1 and significantly inhibited the expression of the inflammatory cytokine IL-6 in chondrocytes. The mitochondrial dynamics imbalance and apoptosis of chondrocytes were increased in the IL-1β group compared with the control group, while the above conditions were ameliorated in the IL-1β+LR12 group. In addition, imbalanced mitochondrial dynamics and increased apoptosis were observed in the TREM1 overexpression group compared with the vector group, which were alleviated in the TREM1 overexpression+LR12 chondrocytes. In addition, PCR Array results indicated that overexpression of TREM1 caused metabolic disturbances in ATDC5 cells. Conclusion: TREM1, to a certain extent, increases imbalance of mitochondrial dynamics and apoptosis of chondrocytes. Targeting TREM1 may provide a new direction for the treatment of osteoarthritis. [ABSTRACT FROM AUTHOR]

Copyright of Journal of China Medical University is the property of Journal of China Medical University Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Preventive Veterinary Medicine / Zhongguo Yufang Shouyi Xuebao is the property of Chinese Journal of Preventive Veterinary Medicine Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To observe the clinical efficacy of bi-level positive airway pressure (BiPAP) in adjuvant treatment of acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and the lung function of patients before and after treatment, Changes in serum inflammatory factors and prognostic indicators. Methods: A total of 150 AECOPD patients admitted to our hospital from August 2017 to July 2020 were selected and divided into a control group and a study group using a random number table method, with 75 cases in each group. The two groups were given basic therapies such as anti-infection, expectorant, correction of water and electrolyte disorders, and nutritional support. On this basis, patients in the control group were given low-flow oxygen inhalation therapy, and patients in the study group were given appropriate masks for BiPAP therapy. The total effective rate of treatment and lung function indexes before and after treatment were compared between the two groups [1 s forced expiratory volume (FEV 1 ), FEV 1 /forced vital capacity (FEV 1 /forced vital capacity, FEV 1 / FVC) and FEV 1 as a percentage of predicted value (FEV 1 as a percentage of predicted value, FEV 1 %)], blood gas indicators [arterial partial pressure of oxygen (PaO2 ) and arterial carbon dioxide partial pressure (arterial partial pressure of carbon dioxide, PaCO 2)], serum inflammatory factors [interleukin-6 (Interleukin-6, IL-6), IL-8 and tumor necrosis factor alpha (TNF-α) levels], soluble myeloid cell trigger receptor-1 (soluble triggering receptor expressed on myeloid cells-1 (s TREM-1) and systemic inflammatory response syndrome (SIRS) quantitative score. Results: The total treatment rate of patients in the study group and control group were 92.00% and 74.67% respectively (P<0.05). After treatment, FEV 1, FEV 1 /FVC, FEV 1 %, PaCO 2, SIRS score, and serum IL-6, IL-8, TNF-α and s TREM-1 levels were significantly lower than before treatment, and PaO 2 was significantly lower after treatment. Higher than before treatment (P<0.05). After treatment in the study group, FEV 1, FEV 1 /FVC, FEV 1 %, PaCO 2, SIRS score, and serum IL-6, IL-8, TNF-α and s TREM-1 levels were significantly lower than those of the control group, and PaO 2 was significantly lower Higher than the control group (P<0.05). Conclusion: BiPAP can improve the clinical efficacy of elderly patients with AECOPD, improve lung function, blood gas level and prognosis, and relieve inflammation. [ABSTRACT FROM AUTHOR]

In recent years, more and more studies have shown that myeloid - derived suppressor cells (MDSCs) participate in the development and progression of various chronic liver diseases including chronic viral hepatitis, alcoholic liver disease, nonalcoholic fatty liver disease, autoimmune liver diseases, and liver cancer. As a type of cells derived from bone marrow progenitor cells and immature myeloid cells, MDSCs play an important role in the development, progression, and repair of liver diseases by regulating inflammatory response and the differentiation and function of immune cells. This article reviews the research advances in the association between MDSCs and various liver diseases, in order to provide new thoughts for the clinical diagnosis, prognosis, and treatment of chronic liver diseases. [ABSTRACT FROM AUTHOR]

Objective: To investigate the role and regulatory mechanism of triggering receptor expressed on myeloid cell 2 (TREM2) in mice lung ischemia/reperfusion injury (LIRI)., Methods: Thirty-six healthy male C57BL/6 mice were divided into six groups according to the random number method (n = 6): normal control group, and LIRI 2, 6, 12, 24, 48 hours group. Mice LIRI models were established by clamping the left hilum. The wet/dry weight ratio (W/D) of left lung tissue was measured. Lung injury was observed and evaluated by hematoxylin-eosin (HE) staining and electron microscopy. The levels of interleukins (IL-1β, IL-18) in lung tissue were detected by enzyme linked immunosorbent assay (ELISA). The mRNA expressions of TREM2 and caspase-1 were determined by polymerase chain reaction (PCR). The protein expressions of TREM2, caspase-1, Gasdermin-D (GSDMD) were determined by Western blotting., Results: At 2 hours after LIRI, lung injury began to appear, the lung ultrastructure changed, and the lung injury score increased; at 6 hours, the degree of lung injury was the most serious; after 12 hours, the lung injury gradually reduced and the lung injury score gradually decreased. Compared with the normal control group, lung W/D ratio and lung injury score of LIRI 2, 6, 12, 24, 48 hours groups were significantly higher, the differences were statistically significant (lung W/D ratio: 7.06±0.52, 8.34±0.17, 6.42±0.35, 5.34±0.25, 5.59±0.45 vs. 4.69±0.23; lung injury score: 5.50±0.54, 9.75±0.89, 5.88±0.84, 3.63±0.74, 4.13±0.64 vs. 1.13±0.35, all P < 0.05). Compared with the normal control group, the levels of IL-1β and IL-18 in lung tissue were significantly increased at 2 hours after LIRI, reached a peak at 6 hours [IL-1β (ng/L): 502.76±12.25 vs. 56.50±8.07, IL-18 (ng/L): 414.02±10.75 vs. 81.63±5.29, both P < 0.05], then decreased gradually, and were still significantly higher than the normal control group at 48 hours. The PCR and Western blotting showed that the expression of TREM2 was significantly lower than that in the normal control group at 2 hours after LIRI, and reached a valley at 6 hours [TREM2 mRNA (2 -ΔΔCt ): 0.47±0.05 vs. 1.02±0.05, TREM2/GAPDH: 0.23±0.13 vs. 0.48±0.17, both P < 0.05], then gradually increased, and reached the peak at 24 hours [TREM2 mRNA (2 -ΔΔCt ): 3.98±0.15 vs. 1.02±0.05, TREM2/GAPDH: 0.71±0.17 vs. 0.48±0.17, both P < 0.05]. The trend of expression of caspase-1 and GSDMD were opposite to that of TREM2, which increased at first and then decreased, and reached a peak at 6 hours after reperfusion [caspase-1 mRNA (2 -ΔΔCt ): 2.20±0.13 vs. 1.01±0.02, caspase-1/GAPDH: 0.64±0.02 vs. 0.20±0.06, GSDMD/GAPDH: 1.23±0.01 vs. 0.87±0.02, all P < 0.05]., Conclusions: TREM2 might be involved in LIRI in mice. The mechanism may be related to the effect of TREM2 on caspase-1-mediated pyroptosis.

Objective: To investigate the relationship between pattern recognition receptor triggering receptors expressed on myeloid cells-1 (TREM-1) and M1/M2 polarization in macrophages stimulated by Porphyromonas gingivalis lipopolysaccharide (Pg-LPS), so as to explore the mechanism of TREM-1 in periodontitis. Methods: Human monocytic cell line THP-1 were induced to differentiate into macrophages by phorbol-12-myristate-13-acetate and stimulated by 0 (blank control group) and 1 μg/ml Pg-LPS (LPS group), respectively. LP17, the TREM-1 inhibitor (LPS+LP17 group) and its control peptide (LPS+control peptide group) with final concentration of 0.1 μg/ml were added at the same time. After 24 hours stimulation, the expression of TREM-1, M1 markers and related cytokines [CD86, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β], M2 markers and related cytokines (CD206,IL-10) mRNA were detected by real-time quantitative-PCR (RT-qPCR), the level of TREM-1, CD86 and CD206 proteins were detected by Western blotting, and TNF-α, IL-1β and IL-10 in the macrophage culture supernatant were detected by enzyme linked immunosorbent assay. Results: After 24 h of cell culture, the relative expressions of TREM-1 mRNA (1.40±0.14) and protein (3.85±0.24) in macrophages in the LPS group increased compared with the blank control group (1.01±0.18 and 1.00±0.05, respectively) ( P <0.05). Meanwhile, the expression levels of M1 markers CD86 mRNA and protein [LPS group vs blank control group were (1.42±0.01 vs 1.00±0.09) and (1.55±0.07 vs 1.00±0.10), respectively] were up-regulated ( P <0.01), and the expressions of mRNA and protein of M1 related cytokines TNF-α and IL-1 increased ( P <0.05). After the addition of TREM-1 blocker LP17, the levels of mRNA and protein of TREM-1 showed no significant changes ( P> 0.05), while the levels of CD86 mRNA (0.96±0.00) and protein (1.36±0.02) decreased ( P <0.05), and the levels of TNF-α and IL-1 further decreased ( P <0.05). For M2 marker CD206 and related cytokine IL-10, CD206 mRNA (0.56±0.05) and protein (0.25±0.04) were significantly down-regulated ( P <0.01) compared with the blank control group (1.02±0.25 and 1.00±0.10, respectively), and IL-10 mRNA was up-regulated compared with the blank control group ( P <0.05), with no significant change in protein ( P >0.05). After the addition of LP17, the expressions of CD206 and IL-10 mRNA in the LPS+LP17 group were further down-regulated compared with the LPS group ( P <0.05), and there was no statistically significant difference between the two groups in protein level ( P >0.05). Conclusions: TREM-1 and its downstream signaling pathway might be involved in M1 polarization of Pg-LPS-mediated macrophages, thus playing a pro-inflammatory role in the development of periodontitis. There is no obvious evidence that TREM-1 is involved in regulating M2 polarization of Pg-LPS-mediated macrophages.

Objective: To evaluate risk factors and available treatments of extramedullary relapse (EMR) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in patients with myeloid leukemia. Methods: A total of 280 patients were retrospectively analyzed from January 2008 to December 2018 in Affiliated Cancer Hospital of Zhengzhou University. Clinical data were collected including disease patterns, pre-transplantation status, chromosome karyotype, conditioning regimen, types of donor, extramedullary disease before transplantation and graft-versus-host disease (GVHD). The log-rank test and Cox proportional hazard model were uesd for univariate analysis and multivariate analysis, respectively. Results: Twenty patients developed EMR (7.14%). The median time of EMR was 7.5 (1-123) months after allo-HSCT. The mortality of EMR was 80% (16/20). Univariate analysis identified disease patterns, second complete remission (CR2) or progressive disease before transplantation, extramedullary disease, abnormal karyotype and conditioning regimen without total body radiation as significant factors correlated to EMR ( P <0.05). Multi-variable analysis revealed that CR2 or progressive disease ( RR =3.468,95% CI 2.189-7.786), abnormal karyotype ( RR =1.494,95% CI 1.020-2.189) and extramedullary disease before transplantation ( RR =8.627,95% CI 3.921-18.452) were independent risk factors of EMR. Conclusions: The clinical outcome of EMR after allo-HSCT is poor.It is crucial to comprehensively assess and identify EMR as early as possible.

Objective: Serum soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) is a useful biomarker of bacterial infection. However, the diagnostic value of sTREM-1 of alveolar fluid in pulmonary infection is still unclear. This article aimed to explore the value of sTREM-1 of alveolar fluid in the early diagnosis of ventilator-associated pneumonia (VAP) by systematic review of relevant literatures., Methods: CNKI, Wanfang, VIP, PubMed/Medline and Embase databases were retrieved. Articles on diagnosis of VAP by sTREM-1 before June 30, 2019 were collected. QUADAS-2 scale provided by Cochrane Collaboration Network was used to evaluate the quality of diagnostic experiments. RevMan 5.3 and Stata 13.0 software were used to complete Meta-analysis. The levels of sTREM-1 between VAP and non-VAP patients were analyzed by Meta-analysis, and then diagnostic test Meta-analysis was conducted. Heterogeneity, sensitivity and publication bias were analyzed., Results: A total of 24 articles were enrolled. QUADAS-2 scale indicated that the selected literature had low bias and high clinical adaptability. (1) In Meta-analysis of sTREM-1 level in alveolar fluid, 20 articles were selected and found to have high heterogeneity (I 2 = 94.4%, P = 0.000). The random effects models were used for Meta-analysis. It was indicated that the sTREM-1 level in alveolar fluid of VAP group was significantly higher than that of non-VAP group with significant difference [standardized mean difference (SMD) was 1.47, 95% confidence interval (95%CI) was 1.00-1.95, Z = 6.14, P = 0.000]. By subgroup analysis and Meta-regression analysis, no source of heterogeneity was found. Sensitivity analysis suggested that the results of this Meta-analysis were robust and credible, and Begg funnel plot analysis showed that there was no significant publication bias (Z = 1.46, P = 0.143). (2) A total of 18 articles were included in the Meta-analysis of diagnostic experiments. Deek funnel plot showed publication bias (P = 0.012). The combined sensitivity was 0.87 (95%CI was 0.81-0.91), specificity was 0.80 (95%CI was 0.73-0.86), and diagnostic odds ratio (DOR) was 26 (95%CI was 13-50). Subgroup analysis of three different sources of alveolar fluid (bronchoalveolar lavage fluid, endotracheal aspiration fluid and exhaled ventilator condensate) showed that STREM-1 had a certain value in early diagnosis of VAP. The I 2 of combined DOR was 35.4%, and I 2 of sensitivity was 79.46%, I 2 of specificity was 77.61%, suggesting heterogeneity in the selected literature. Subgroup analysis found that nationality, subject design, sample source, sample size and diagnostic "gold criteria" were related to heterogeneity, but not age. The area under synthetic receiver operating characteristic (SROC) curve (AUC) was 0.90 (95%CI was 0.87-0.92)., Conclusions: The detection of sTREM-1 level in alveolar fluid can be used for the early diagnosis of VAP with high sensitivity and specificity. If combined with other biomarkers, it may have more diagnostic value.

Objective: Soluble triggering receptors expressed by myeloid cells-1 (sTREM-1) and inflammatory cytokine tumor necrosis factor-α (TNF-α) in macrophage cells were stimulated by Porphyromonas gingivalis-lipopolysaccharide (Pg-LPS) to investigate the expression of triggering receptors expressed by myeloid cells-1 (TREM-1) and further explore the correlation between TREM-1 and the pathogenesis of periodontitis., Methods: THP-1 cells (a human monocytic cell line derived from an acute monocytic leukemia patient) were induced to differentiate THP-1 macrophages by phorbol-12-myristate-13-acetate and were injected with 0 (blank control), 0.5, or 1.0 μg·mL⁻¹ Pg-LPS. The THP-1 cells were then grouped in accordance with incubation time, and each group was incubated for 4, 6, 12, or 24 h. The expression of the TREM-1 mRNA in macrophages was detected by real-time quantitative polymerase chain reaction, while the expression of TREM-1 protein was detected by Western blot; the site where TREM-1 protein expression was observed in macrophages was detected by immunofluorescence staining, and the expression of soluble sTREM-1 and TNF-α in cell culture medium was detected by enzyme-linked immunosorbent assay., Results: Compared with the blank control group, the expression of TREM-1 mRNA, TREM-1 protein, and sTREM-1 in Pg-LPS-stimulated macrophages was significantly upregulated (P<0.05). The expression of TREM-1 mRNA, TREM-1 protein, and sTREM-1 in the supernatant of cell culture was higher in the 1.0 μg·mL⁻¹ Pg-LPS group than in the 0.5 μg·mL⁻¹ group; this expression was statistically significant since the 6, 4, and 4 h time point (P<0.05). Cell immunofluorescence staining showed that TREM-1 protein was positive when the THP-1 macrophages was stimulated by Pg-LPS (1.0 μg·mL⁻¹) for 24 h, and the staining sites of TREM-1 were mainly located in the cell membrane of the macrophages (P<0.05). The expression level of TNF-α increased in groups stimulated by Pg-LPS, and the expression level of TNF-α was significantly higher in 1.0 μg·mL⁻¹ Pg-LPS stimulated groups than in 0.5 μg·mL⁻¹ Pg-LPS-stimulated groups since the 6 h time point (P<0.05). The expressions of TREM-1 mRNA, TREM-1 protein, and sTREM-1 in 0.5 μg·mL⁻¹ Pg-LPS-stimulated macrophages were positively correlated with one another (r=1, P<0.05), but no statistically significant correlation was found in the expression of TNF-α. The positive correlation between sTREM-1 and TNF-α expressions was detected when macrophages were stimulated by 1.0 μg·mL⁻¹ Pg-LPS (r=1, P<0.05)., Conclusions: The expression of TREM-1 mRNA, TREM-1 protein, and sTREM-1 in the culture supernatant in Pg-LPS-stimulated macrophages was significantly upregulated on the basis of the concentration of Pg-LPS; moreover, their upregulation was positively correlated with one another. The expression of TNF-α in the supernatant of cell culture was also upregulated and was positively correlated with the expression of sTREM-1 at the group of high Pg-LPS concentration (1.0 μg·mL⁻¹). Results reveal that TREM-1, which has been realized as a proinflammatory receptor protein, can promote the development of periodontitis by regulating the expression of TNF-α in macrophages.

Increasing scientific evidence supports the positive relationship between inflammation and cancer development. The immune response initiated by pattern recognition receptors is critical to triggering of tumor-associated inflammation. Triggering receptor expressed on myeloid cells (TREM) is an immunoglobulin of the super transmembrane glycoprotein family, which is mainly expressed on select groups of myeloid cells. The most important members of TREM comprise TREM-1 and TREM-2. Activation of TREM-1 and TREM-2 signaling is initiated upon binding of their ligands. Subsequently, cross-linking reactions of downstream effectors occur, resulting in inflammation regulation. Recently, the connection between TREM and malignant tumors has been widely noticed and studied. This review summarizes studies of association between TREM-1, TREM-2, and malignant tumors in the medical field to provide new ideas for study on the correlation between periodontitis and oral cavity cancer.

Objective: To investigate the expression of triggering receptor expressed on myeloid cells receptor-1 (TREM-1) in plasma and bronchoalveolar lavage fluid (BALF) and its correlation with Galactomannan, IFNγ, IL-6 and IL-10 in Aspergillus infected mice. Methods: Cyclophosphamide(CTX) was intraperitoneally injected and fumigatus spore suspension was inhaled by nose to establish the immunocompromised invasive pulmonary aspergillosis(IPA) mouse model.Healthy controls, immunocompromised only and IPA only groups were also established. Each group had 6 mice. After inoculation, mice were sacrificed. Lung tissue specimens, BALF, and plasma samples were collected. Plasma and BALF soluble TREM-1 (sTREM-1), Galactomannan, IFNγ, IL-6, and IL-10 were detected by ELISA. Results: Positive Aspergillus fumigatus was found by tissue culture in the lung. Infiltration of inflammatory cells, blood congestion and interstitial lung tissue injury were observed in histological sections of both IPA and immunocompromised IPA mice. Compared to IPA group [(453.78±74.18) ng/L, P <0.001; (10.21±1.46) ng/L, P <0.001] and control group [(245.16±65.85) ng/L, P <0.001; (6.60±3.74) ng/L, P <0.001], the plasma and BALF sTREM-1 significantly increased in immunocompromised IPA group [(1 537.64±359.52) ng/L; (20.12±2.72) ng/L]. Compared to control group, both the BALF sTREM-1 in IPA group ( P =0.041) and the plasma and BALF Galactomannan, IFNγ, IL-6, and IL-10 levels in IPA and immunocompromised IPA groups were significantly higher ( P <0.01). Pearson correlation analysis showed that plasma and BALF sTREM-1 were significantly correlated with Galactomannan ( r =0.83, P <0.001; r =0.82, P <0.001), IFNγ ( r =0.79, P <0.001; r =0.61, P <0.01), IL-6 ( r =0.81, P <0.001; r =0.66, P <0.01), and IL-10 ( r =0.70, P =0.001; r =0.54, P =0.02). Conclusions: Plasma and BALF sTREM-1 appears highly expressed in Aspergillus infected mice. sTREM-1 in mice plasma and BALF is closely correlated with Galactomannan, IFNγ, IL-6, and IL-10 levels, which suggests that sTREM-1 has great diagnostic value during invasive fungal infection.

Objective: To investigate the function of triggering receptor expresses on myeloid cells receptor-1 (TREM-1) in lymphocyte differentiation and regulation of Aspergillus infected immunosuppressed rats., Methods: Cyclophosphamide (CTX) was intraperitoneally injected and Fumigatus spore suspension was inhaled by percutaneous tracheostomy to establish the immunosuppressive invasive pulmonary aspergillosis (IPA) rat model. After 24 h, 48 h, 72 h and 96 h inoculation, rats were sacrificed. Lung tissue specimens, bronchoalveolar lavage fluid (BALF), and plasma samples were collected. Plasma and BALF sTREM-1, plasma T cell-specific transcription factor (T-box expressed in T cells, T-bet) and eomesodermin(Eomes) were detected by ELISA. Biopsy specimens of lung tissue were used for periodic acid-schiff (PAS) staining and culture., Results: The mortality rate of immunosuppressed rats after Aspergillus inhalation for 96 h was as high as 54.4%. Biopsy of lung tissue suggested acute inflammatory cell infiltration, interstitial lung congestion, alveolar structural damage, and visible Aspergillus hyphae in alveoli. Compared with normal control group[(110.50 ± 7.70) ng/L], plasma sTREM-1 in study groups were significantly increased[IPA: (146.77 ± 10.41) ng/L; CXT+ IPA at 24 h: (226.00 ± 11.88) ng/L; CTX+ IPA at 48 h: (200.77 ± 10.63) ng/L; P<0.05], so were T-bet levels[IPA: (561.17 ± 7.23) μg/L; CXT+ IPA at 24 h: (647.00 ± 33.03) μg/L; CTX+ IPA at 48 h: (619.23 ± 87.44) μg/L; control group: (340.03 ± 26.32) μg/L; respectively, P < 0.05]. However, plasma Eomes levels in IPA group, CTX+ IPA at 24 h and 48 h were significantly lower compared with that in normal controls[IPA: (7.96 ± 0.65) ng/L; CXT+ IPA at 24 h: (3.97 ± 0.35) ng/L; CTX+ IPA at 48 h: (4.00 ± 0.74) ng/L; control group: (8.38 ± 0.51) ng/L; respectively, P < 0.001]. Compared with those in CTX+ IPA vaccination after 24 h and 48 h, plasma sTREM-1 [(106.67 ± 7.64) ng/L; (133.27 ± 32.79) ng/L] and T-bet [(299.64 ± 63.07) μg/L; (398.02 ± 109.22) μg/L] in CTX+ IPA at 72 h and 96 h inoculation were significantly lower (P < 0.001). While Eomes [(8.38 ± 0.54) ng/L; (8.40 ± 0.70) ng/L]raised significantly higher (P < 0.001). Compared with the control group, sTREM-1 levels in BALF of IPA+ CTX 24 h, 48 h, 72 h, and 96 h groups were consistently high (P < 0.05). Pearson correlation analysis showed that sTREM-1 and T-bet had a significant positive correlation (r = 0.91, P < 0.001), yet Eomes was negatively correlated with them (r = -0.788, P < 0.001)., Conclusions: sTREM-1 in rat plasma and BALF appears highly expressed in immune compromised Aspergillus infected rat model. Plasma sTREM-1 is closely correlated with T-bet and Eomes levels, which suggests that TREM-1 may be involved in lymphocytic regulation and differentiation during fungal infection.

Objective: To investigate the effects of microRNA-294 (miR-294) on tumor necrosis factor-α (TNF-α), interleukin -6 (IL-6) and high mobility group box 1 (HMGB1) secretion in sepsis by targeting triggering receptor expressed on myeloid cell-1 (TREM-1)., Methods: miRNA-294 was predicted to regulate TREM-1 specially through bioinformatics analysis. Mice macrophage cell lines RAW264.7 were cultured in vitro, the cells were divided into non-inflammatory stage and inflammatory stage, and the cells in the two stages were subdivided into five groups as follows: normal control (NC), NC mimic transfection (NCm), NC inhibitor transfection (NCi), miR-294 mimic transfection (miR-294 m) and miR-294 inhibitor transfection (miR-294i) groups. The ability of miR-294 was confirmed with dual-luciferase activity assay. At non-inflammatory stage, the cells were transfected with mimic or inhibitor of miR-294 or NC using TurboFect™ siRNA Transfection Reagent for 48 hours, mRNA expression of TREM-1 was detected by real-time reverse transcription-polymerase chain reaction (RT-PCR). At inflammatory stage, 6 hours after stimulation by lipopolysaccharide (LPS, 1 mg/L), the concentrations of TNF-α, IL-6 and HMGB1 were determined by enzyme linked immunosorbent assay (ELISA), the protein expression of TREM-1 was determined by Western Blot., Results: (1) Dual-luciferase activity assay demonstrated that TREM-1 was the target of miR-294. (2) In non-inflammatory stage, the expression of TREM-1 mRNA (2(-ΔΔCt) ) in miR-294m group was significantly lower than that of the NC and NCm groups (0.673 ± 0.049 vs. 1.000 ± 0.003, 0.915 ± 0.039, t1=2.184, t2=5.421, both P<0.001), the expression of TREM-1 protein (gray scale) was (50.00 ± 1.19)% of NCm group (t=41.586, P<0.001). (3) In inflammatory stage, the concentrations of TNF-α (ng/L) in miR-294 m group was significantly lower than that of the NC group (1 547.18 ± 47.18 vs. 2 702.11 ± 327.20, t=4.212, P=0.010), the concentrations of IL-6 (ng/L) was significantly lower than that of the NC and NCm groups (505.28 ± 33.33 vs. 837.66 ± 69.43, 918.72 ± 119.39, t1=4.382, P1=0.015; t2=5.451, P2=0.021), the level of TREM-1 protein(gray scale) was (51.33 ± 0.88)% of NCm group (t=63.368, P<0.001)., Conclusions: miR-294 reduce TNF-α and IL-6 secretion in LPS-induced RAW264.7 through inhibiting the expression of TREM-1 specifically.

Objective: To explore the presence, frequency and clinical value of myeloid-derived suppressor cells (MDSCs) in peripheral blood of patients with small cell lung cancer (SCLC)., Methods: Flow cytometry using antibodies against CD11b, CD33, CD14 or HLA-DR was conducted to explore the unique cell surface markers of MDSCs and statistical analysis was performed to explore the correlation of MDSCs and clinical features., Results: MDSCs were present in 36 patients with SCLC and uniquely marked by CD11b and CD33-positive, but HLA-DR-negative on cell surfaces and possessed mononuclear phenotype. The levels of CD11b(+)CD33(+)HLA-DR(-)cells (MDSCs) in the SCLC patients and healthy controls were (26.87 ± 6.87)% and (11.04 ± 3.76)%, respectively, with a statistically significant difference (P < 0.001). MDSCs level was significantly associated with clinical stage and tumor distant metastasis (P < 0.05) , but not with age, sex, smoking status and performance status. The later was the clinical stage, the higher was the MDSCs level (r = 0.665, P < 0.001). The level of MDSCs was higher in SCLC patients with distant metastasis than in those without metastasis (r = 0.489, P = 0.003). The level of MDSCs was higher before treatment than after treatment and the difference was statistically significant (P = 0.003)., Conclusions: The results of our study demonstrate the existence of MDSCs in SCLC patients and the MDSCs level is associated with SCLC stage, metastasis and treatments. MDSCs might be a novel biomarker for early diagnosis and prognosis for SCLC patients.

Objective: To study the effect of Weiganli on the level of FL in bone marrow and serum of myelosuppressed anemic mice, and to explore it's function on hematopoietic regulation., Method: Models of myelosuppressed anemic mice were induced by radiation and chemotherapeutic drug, and the mice were randomly divided into normal group, myelosuppressed anemic group, and Weiganli group (high dose 100 g x L(-1), medium dose 50 g x L(-1), low dose 25 g x L(-1)). Effect of Weiganli on the number of the peripheral blood cells and bone marrow nucleated cells (BMC) were evaluated. Effect of Weiganli on the level of FL (Flt3 ligand) was investigated by ELISA technique., Result: High dose of Weiganli could significantly increase granulocytes, erythrocytes, Hb and BMC, while both the medium dose and the low dose had more significant action in increase of platelet. The level of FL in bone marrow and serum were lower in Weiganli group than that in myelosuppressed anemic group, especially in high and medium dose group., Conclusion: The myelosuppresion of mice which induced by radiation and chemotherapeutic drug could be significantly relieved by Weiganli.

Objective: To investigate the expression of triggering receptor expressed on myeloid cells (TREM-1) in monocytes of burn patients at early post-burn stage, and its significance., Methods: The monocytes of 8 healthy volunteers (A group), 29 patients with mild and moderate burn (B group), and 9 patients with severe and very serious burns (C group) were isolated from the blood, and the THEM-1 mRNA and protein expression were determined by semi-quantitative RT-PCR and flow cytometry, respectively. The plasma levels of TNF-alpha, IL-1beta were determined by ELISA method., Results: The value of TREM-1 mRNA expression in A, B and C groups were 0.74 +/- 0.13, 1.24 +/- 0.09, and 1.46 +/-0.07, respectively, and the expression rates on cell surface in the 3 groups were (9 +/- 4)%, (51 +/- 6)%, and (71 +/- 7)%, respectively, and there were significant differences among the three groups (P = 0.000). the plasma levels of TNF-alpha and IL-1beta in B and C groups were obviously higher than that in A group (P = 0.000), and they were positively correlated to TREM-1 expression (rs = 0.68, 0.72, P = 0.000)., Conclusion: Increased expression of TREM-1 in monocytes of burn patients at early post-burn stage is correlated with the release of inflammatory factors, indicating that TREM-1 might contribute to the onset and development of acute inflammatory response after burns.