Search

Currently, there's a lack of research on air volume regulation and mine resistance reduction of ventilation system in mine working face. In order to solve the above problem, taking 10303 working face and 33low 02 working face of Jining No.2 Coal Mine as the engineering background, the original ventilation systems in these two areas are optimized and transformed in terms of air volume regulation and mine resistance reduction. The ventilation system diagram of the working face is imported into Ventism software, generating a solid roadway and iterating the calculation to construct a mine ventilation network solution model. The main parameters measured on-site are input into the model for airflow calculation. The errors between calculated relevant data such as flow velocity, temperature, and air volume in the roadway obtained and the on-site measurement data are within the standard range. From the measurement results of mine ventilation resistance, it can be seen that the original ventilation system has the following problems. The setting of the regulating air wall at the south wing stone gate is unreasonable. The actual air supply volume of 33low02 working face is less than the ideal air volume. The ventilation route of the south wing -740 horizontal track main roadway is long. It is affected by the parallel intake of auxiliary transportation roadways, resulting in high resistance in the south wing return air main roadway. In order to solve the above problems, three renovation measures are proposed. ① A closed air door is installed at the intersection of the south wing return air stone gate and the north wing belt conveyor roadway. The original air window area of the south wing belt conveyor roadway and return air stone gate is adjusted to 2.9 m2. ② A 0.1 m2 adjustable wind window is installed at the intersection of the extension of the third mining area's track downhill and the 33low02 connecting roadway. ③ The 0.9 m2 adjustable air window at the interface between the pipe duct in the 11th mining area and the south wing -740 horizontal track roadwayhas been changed to 2.4 m2,so as to reduce the air volume of the south wing -740 horizontal track roadway and increase the parallel air volume of the auxiliary transportation roadway. The simulation results of the modified ventilation system show that the resistance of the southern wing -740 horizontal track main roadway has been reduced by 32.7%. The air volume of the 33low02 working face has been increased by 19.8%. The total resistance of the mine ventilation route has been reduced by 6.4%. The on-site measurement results of the modified ventilation system show that the average relative error between the measured air volume and numerical simulation results is 1.28%. The average relative error between the measured resistance and numerical simulation results is 2.52%. The optimized simulation results are basically consistent with the on-site test results. The range of changes in air volume and resistance of the intake shaft before and after the entilation system adjustment is not significant. The air volume at the measuring point of the return air shaft decreases, and resistance decreased. The optimized measured air volume at the 33low02 track connecting roadway and the measuring points of the working face increase by 25.3% and 21.4%, respectively, and the resistances increase by 57.4% and 41.1%. The optimized measured air volume at the south wing -740 horizontal track roadway decreases by 20.3%, and resistance decreases by 36.6%. After the renovation, the air volume of the working face and the total resistance of the mine have achieved the expected results.

Background: Current strategies in circulating tumor cell (CTC) isolation in pancreatic cancer heavily rely on the EpCAM and cytokeratin cell status. EpCAM is generally not considered a good marker given its transitory change during Epithelial to Mesenchymal Transition (EMT) or reverse EMT. There is a need to identify other surface markers to capture the complete repertoire of PDAC CTCs. The primary objective of the study is to characterize alternate surface biomarkers to EpCAM on CTCs that express low or negligible levels of surface EpCAM in pancreatic cancer patients. Methods: Flow cytometry and surface mass spectrometry were used to identify proteins expressed on the surface of PDAC CTCs in culture. CTCs were grown under conditions of attachment and in co-culture with naïve neutrophils. Putative biomarkers were then validated in GEMMs and patient samples. Results: Surface proteomic profiling of CTCs identified several novel protein biomarkers. ALCAM was identified as a novel robust marker in GEMM models and in patient samples. Conclusions: We identified several novel surface biomarkers on CTCs expressed under differing conditions of culture. ALCAM was validated and identified as a novel alternate surface marker on EpCAMlow CTCs. [ABSTRACT FROM AUTHOR]

Microcystin-LR (MC-LR), the most common and toxic microcystin (MC) present in freshwater, poses a substantial threat to human health, especially hepatotoxicity. Recent evidence reveals that the NLRP3 inflammasome plays an important role in liver injury by activating caspase-1 to promote interleukin-1β (IL-1β) secretion. In this study, we investigated the possible role of NLRP3 inflammasome activation in MC-LR-induced mouse liver inflammatory injury. We found that MC-LR administered to mice by oral gavage mainly accumulated in liver and induced the activation of the NLRP3 inflammasome and production of mature IL-1β. Additionally, we observed an increase in the levels of NLRP3 inflammasome-related proteins and the proportion of pyroptosis in MC-LR-treated AML-12 cells. We also found that inhibition of NLRP3 in mice attenuated MC-LR-induced IL-1β production, indicating an essential role for NLRP3 in MC-LR-induced liver inflammatory injury. In addition, we found that inhibition of FOXO1 by AKT-mediated hyperphosphorylation, due to protein phosphatase 2A (PP2A) inhibition, is required for MC-LR-induced expression of NLRP3. Taken together, our in vivo and in vitro findings suggest a model in which the NLRP3 inflammasome activation, a result of AKT-mediated hyperphosphorylation of FOXO1 through inhibition of PP2A, plays a key role in MC-LR–induced liver inflammatory injury via IL-1β secretion and pyroptotic cell death. [ABSTRACT FROM AUTHOR]

Extracellular vesicles (EVs) from biofluids have recently gained significant attention in the field of liquid biopsy. Released by almost every type of cell, they provide a real-time snapshot of host cells and contain a wealth of molecular information, including proteins, in particular those with post-translational modifications (PTMs) such as phosphorylation, as the main player of cellular functions and disease onset and progression. However, the isolation of EVs from biofluids remains challenging due to low yields and impurities from current EV isolation methods, making the downstream analysis of EV cargo, such as EV phosphoproteins, difficult. Here, we describe a rapid and effective EV isolation method based on functionalized magnetic beads for EV isolation from biofluids such as human urine and downstream proteomics and phosphoproteomics analysis following EV isolation. The protocol enabled a high recovery yield of urinary EVs and sensitive profiles of EV proteome and phosphoproteome. Furthermore, the versatility of this protocol and relevant technical considerations are also addressed here.

Purpose: To compare the efficacy and impact of GEMOX and GDP in the treatment of patients with non-Hodgkin's lymphoma (NHL)., Methods: A total of 68 patients with NHL admitted to the hospitals of the authors from February 2013 to April 2016 were equally distributed into the GEMOX Group (treated with Gemcitabine and Oxaliplatin) and the GDP Group (treated with Gemcitabine, Cisplatin, and Dexamethasone), with cycle repetition every 3 weeks. The efficacy was analyzed every two weeks. The side effects were analyzed once a week. Comparison of survival was performed using Kaplan-Meier method and log-rank test and Cox univariate and multivariate regression analyses., Results: Efficacy in the two groups was not statistically different (p>0.05). The incidence of III-IV grade of nausea and vomiting in the GDP Group was higher than in the GEMOX Group (p<0.05). The overall incidence decreased hemoglobin, nausea and vomiting, and renal dysfunction of the GDP Group was also higher than in the GEMOX Group (p<0.05). Analysis by multivariate Cox model found that the clinical classification and the grade of malignancy were independent prognostic factors (p<0.05). The odds ratio (OR) values of the clinical classification in the GEMOX Group and the GDP Group were 2.874 and 24.074, respectively. The OR values of the grade of malignancy in the GEMOX Group and the GDP Group were 14.034 and 6.873, respectively., Conclusion: Both the GEMOX regimen and the GDP regimen had good short-term efficacy on NHL patients, but the GEMOX regimen is to be preferred since as it had fewer side effects than the GDP regimen.

Myogenic regulatory factors (MRFs), including Myf5, MyoD (Myod1) and Myog, are muscle-specific transcription factors that orchestrate myogenesis. Although MRFs are essential for myogenic commitment and differentiation, timely repression of their activity is necessary for the self-renewal and maintenance of muscle stem cells (satellite cells). Here, we define Ascl2 as a novel inhibitor of MRFs. During mouse development, Ascl2 is transiently detected in a subpopulation of Pax7 + MyoD + progenitors (myoblasts) that become Pax7 + MyoD - satellite cells prior to birth, but is not detectable in postnatal satellite cells. Ascl2 knockout in embryonic myoblasts decreases both the number of Pax7 + cells and the proportion of Pax7 + MyoD - cells. Conversely, overexpression of Ascl2 inhibits the proliferation and differentiation of cultured myoblasts and impairs the regeneration of injured muscles. Ascl2 competes with MRFs for binding to E-boxes in the promoters of muscle genes, without activating gene transcription. Ascl2 also forms heterodimers with classical E-proteins to sequester their transcriptional activity on MRF genes. Accordingly, MyoD or Myog expression rescues myogenic differentiation despite Ascl2 overexpression. Ascl2 expression is regulated by Notch signaling, a key governor of satellite cell self-renewal. These data demonstrate that Ascl2 inhibits myogenic differentiation by targeting MRFs and facilitates the generation of postnatal satellite cells., (© 2017. Published by The Company of Biologists Ltd.)