Research on AGC control performance optimization and application of 135MW coal-fired unit

This paper studies the corresponding performance optimization of unit coordinated control system. Combined with the actual operation of the unit, targeted optimization strategies are formulated and implemented for the main parameters such as active power, main steam pressure, feed water flow, main steam temperature and furnace pressure. After long-term tracking of operation and repeated adjustment of relevant control parameters, a more reasonable optimization effect is finally obtained, and the regulation performance of the unit coordinated control system meets the AGC input conditions

Potentilla parvifolia strongly influenced soil microbial community and environmental effect along an altitudinal gradient in central Qilian Mountains in western China

Abstract The Qilian Mountains (QLMs) form an important ecological security barrier in western China and a priority area for biodiversity conservation. Potentilla parvifolia is a widespread species in the mid‐high altitudes of the QLMs and has continuously migrated to higher altitudes in recent years. Understanding the effects of P. parvifolia on microbial community characteristics is important for exploring future changes in soil biogeochemical processes in the QLMs. This study found that P. parvifolia has profound effects on the community structure and ecological functions of soil microorganisms. The stability and complexity of the root zone microbial co‐occurrence network were significantly higher than those of bare soils. There was a distinct altitudinal gradient in the effect of P. parvifolia on soil microbial community characteristics. At an elevation of 3204 m, P. parvifolia promoted the accumulation of carbon, nitrogen, and phosphorus and increased sucrase activity and soil C/N while significantly improving the community richness index of fungi (p < .05) compared with that of bacteria and the relative abundance of Ascomycota. The alpha diversity of fungi in the root zone soil of P. parvifolia was also significantly increased at 3550 m altitude. Furthermore, the community similarity distance matrix of fungi showed an evident separation at 3204 m. However, at an altitude of 3750 m, P. parvifolia mainly affected the bacterial community. Potentilla parvifolia increased the bacterial community richness. This is in agreement with the findings based on the functional prediction that P. parvifolia favors the growth and enrichment of denitrifying communities at 3550 and 3750 m. The results provide a scientific basis for predicting the evolutionary trends of the effects of P. parvifolia on soil microbial communities and functions and have important implications for ecological governance in the QLMs

Hyperglycemia aggravates microenvironment hypoxia and promotes the metastatic ability of pancreatic cancer

Background: Diabetes mellitus and pancreatic cancer are intimately related. Our previous studies showed that high levels of blood glucose promote epithelial-mesenchymal transition of pancreatic cancer. In this study, we evaluated the relationship between hyperglycemia and hypoxic tumor microenvironments. Methods: HIF-1α expression was evaluated by immunohistochemistry in clinical pancreatic cancer tissues with or without diabetes mellitus. Statistcal analysis was performed to explore the relationship between HIF-1α expression and pathological features of patients with pancreatic cancer. In vivo and in vitro models was established to detect whether a hyperglycemia environment could cause hypoxia in the pancreatic parenchyma and promote pancreatic cancer. In addition, we also tested the effect of HIF-1α siRNA on the high glucose-induced invasive and migratory abilities of BxPC-3 cells in culture. Result: Our data showed that pancreatic cancer patients with diabetes had a higher level of HIF-1α expression as well as biliary duct invasion and larger tumor volumes than individuals in the euglycemic group. Diabetic nude mice treated with streptozotocin (STZ) exhibited larger tumors and were more likely to develop liver metastasis than control mice. Acinar cells of the pancreas in diabetic mice showed an obvious expansion of the endoplasmic reticulum and increased nuclear gaps as well as chromatin close to the cellular membrane in some acinar cells. The expression area for Hypoxyprobe-1 and HIF-1α in the diabetic orthotopic xenograft group was larger than that in the control group. The expression level of HIF-1α in the BxPC-3 cancer cell line increased in response to high glucose and CoCl2 concentrations. The high glucose-induced invasive ability, migratory capacity and MMP-9 expression were counter-balanced by siRNA specific to HIF-1α. Conclusion: Our results demonstrate that the association between hyperglycemia and poor prognosis can be attributed to microenvironment hypoxia in pancreatic cancer. Keywords: Hyperglycemia, Hypoxia, HIF-1α, Metastasis, Pancreatic cance

Enhanced performance of lithium-sulfur batteries with high sulfur loading utilizing ion selective MWCNT/SPANI modified separator

Lithium-sulfur (Li-S) battery has attracted remarkable attention owing to its high theoretical energy density. However, its commercialization is still hampered by the rapid capacity degradation which mainly originates from the polysulfides shuttle between the anode and cathode. In this paper, a functional multiwall carbon nanotube/sulfonated polyaniline (MWCNT/SPANI) modified separator is designed to enhance the electrochemical performance of the Li-S batteries with high sulfur loading. The MWCNT/SPANI-coated separator is highly permselective to Li+ but rejects the transportation of polysulfide anions. Besides, the MWCNT/SPANI coating can also work as an upper current collector and provides channels for electron and ion transport to enhance the sulfur utilization and ensure the reactivation of trapped active materials. With the ion selective MWCNT/SPANI-coated separator, the electrochemical performance of the Li-S batteries based on cathodes with high sulfur loading (5 mg cm−2) and high sulfur content (72 wt%) has been significantly improved. It delivers a reversible capacity of 913 mA h g−1 at the current density of 100 mA g−1 after 100 cycles, much higher than that of the cells with pristine Celgard separator. Hence, the ion selective MWCNT/SPANI modified separator is promising for developing high-performance Li-S batteries employing cathodes with high sulfur loading and high sulfur content

Resveratrol-Induced Downregulation of NAF-1 Enhances the Sensitivity of Pancreatic Cancer Cells to Gemcitabine via the ROS/Nrf2 Signaling Pathways

NAF-1 (nutrient-deprivation autophagy factor-1), which is an outer mitochondrial membrane protein, is known to play important roles in calcium metabolism, antiapoptosis, and antiautophagy. Resveratrol, a natural polyphenolic compound, is considered as a potent anticancer agent. Nevertheless, the molecular mechanisms underlying the effects of resveratrol and NAF-1 and their mediation of drug resistance in pancreatic cancer remain unclear. Here, we demonstrate that resveratrol suppresses the expression of NAF-1 in pancreatic cancer cells by inducing cellular reactive oxygen species (ROS) accumulation and activating Nrf2 signaling. In addition, the knockdown of NAF-1 activates apoptosis and impedes the proliferation of pancreatic cancer cells. More importantly, the targeting of NAF-1 by resveratrol can improve the sensitivity of pancreatic cancer cells to gemcitabine. These results highlight the significance of strategies that target NAF-1, which may enhance the efficacy of gemcitabine in pancreatic cancer therapy

Resveratrol Inhibits ROS-Promoted Activation and Glycolysis of Pancreatic Stellate Cells via Suppression of miR-21

Activation of pancreatic stellate cells (PSCs) initiates pancreatic fibrosis in chronic pancreatitis and furnishes a niche that enhances the malignancy of pancreatic cancer cells (PCCs) in pancreatic ductal adenocarcinoma (PDAC). Resveratrol (RSV), a natural polyphenol, exhibits potent antioxidant and anticancer effects. However, whether and how RSV influences the biological properties of activated PSCs and the effects of these changes on tumor remain unknown. In the present study, we found that RSV impeded hydrogen peroxide-driven reactive oxygen species- (ROS-) induced activation, invasion, migration, and glycolysis of PSCs. In addition, miR-21 expression in activated PSCs was downregulated after RSV treatment, whereas the PTEN protein level increased. miR-21 silencing attenuated ROS-induced activation, invasion, migration, and glycolysis of PSCs, whereas the overexpression of miR-21 rescued the responses of PSCs treated with RSV. Moreover, RSV or N-acetyl-L-cysteine (NAC) administration or miR-21 knockdown in PSCs reduced the invasion and migration of PCCs in coculture, and the effects of RSV were partly reversed by miR-21 upregulation. Collectively, RSV inhibits PCC invasion and migration through suppression of ROS/miR-21-mediated activation and glycolysis in PSCs. Therefore, targeting miR-21-mediated glycolysis by RSV in tumor stroma may serve as a new strategy for clinical PDAC prevention or treatment

44° Convegno Nazionale Associazione Italiana di Acustica

Abstract Background Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer-associated mortality worldwide with an overall five-year survival rate less than 7%. Accumulating evidence has revealed the cancer preventive and therapeutic effects of metformin, one of the most widely prescribed medications for type 2 diabetes mellitus. However, its role in pancreatic cancer is not fully elucidated. Herein, we aimed to further study the preventive and therapeutic effects of metformin in genetically engineered mouse models of pancreatic cancer. Methods LSL-KrasG12D/+; Pdx1-Cre (KC) mouse model was established to investigate the effect of metformin in pancreatic tumorigenesis suppression; LSL-KrasG12D/+; Trp53fl/+; Pdx1-Cre (KPC) mouse model was used to evaluate the therapeutic efficiency of metformin in PDAC. Chronic pancreatitis was induced in KC mice by peritoneal injection of cerulein. Results Following metformin treatment, pancreatic acinar-to-ductal metaplasia (ADM) and mouse pancreatic intraepithelial neoplasia (mPanIN) were decreased in KC mice. Chronic pancreatitis induced a stroma-rich and duct-like structure and increased the formation of ADM and mPanIN lesions, in line with an increased cytokeratin 19 (CK19)-stained area. Metformin treatment diminished chronic pancreatitis-mediated ADM and mPanIN formation. In addition, it alleviated the percent area of Masson’s trichrome staining, and decreased the number of Ki67-positive cells. In KPC mice, metformin inhibited tumor growth and the incidence of abdominal invasion. More importantly, it prolonged the overall survival. Conclusions Metformin inhibited pancreatic cancer initiation, suppressed chronic pancreatitis-induced tumorigenesis, and showed promising therapeutic effect in PDAC