Search

Nitrogen-doped modified activated carbons (ACs) were prepared from coconut shell, date shell and almond shell using the urea modification method. NO tests of NH3 selective catalytic reduction (NH3-SCR) were conducted to evaluate the efficiency of different types of nitrogen-doped modified AC as denitration catalyst carriers between 50–220°C. Both AC and nitrogen-doped modified AC had catalytic effects on NO conversion; the nitrogen-doped modified AC had high denitrification activity in the low-temperature region, and NAC1-10 achieved an NO conversion rate of 65.7% at 50°C. The low-temperature denitrification activity of urea-modified AC was twice that of the untreated AC at all temperatures. The O2 concentration in the SCR reaction system had a significant effect on the NO conversion rate of the nitrogen-doped modified AC. As the O2 concentration increased from 0 to 1 vol%, the NO conversion rate increased rapidly from 22 to 65% and remained stable at 65%. A series of characterisation tools were used to determine the structure and physicochemical properties of the nitrogen-doped modified AC, including BET, XRD, elemental analysis, and FTIR. Nitrogen-doped AC showed good air velocity adaptability and low-temperature stability, suggesting that it is a promising carrier for NH3-SCR catalysts. Nitrogen-doped modified activated carbons (NACs) were prepared from coconut shell, date shell, and almond shell using the urea modification method. NO tests of NH3 selective catalytic reduction (NH3-SCR) were conducted to evaluate the efficiency of different types of nitrogen-doped modified AC as denitration catalyst carriers at 50–220°C. NACs denitrification activity tests were carried out in a fixed-bed reactor with an inner diameter of 15 mm and a total gas flow rate of 500 mL·min−1 flue gas. [ABSTRACT FROM AUTHOR]

Renal ischaemia/reperfusion (I/R) is a major cause of acute renal failure with increased morbidity, mortality, and prolonged hospitalizations. Clematichinenoside (AR), a triterpenoid saponin isolated from the roots of Clematis chinensis, was reported to possess a protective effect against I/R injury. However, the effect of AR on renal I/R injury has not been evaluated. This study aims to examine the effect of AR on an in vitro I/R model in human proximal tubular epithelial cells HK‐2. HK‐2 cells were subjected to hypoxia/reoxygenation (H/R) stimulation to mimic I/R in vitro. The results showed that AR improved cell viability of H/R‐stimulated HK‐2 cells. AR pretreatment resulted in decreased production of reactive oxygen species (ROS) and malondialdehyde (MDA), as well as increased in superoxide dismutase (SOD) activity in H/R‐stimulated HK‐2 cells. In addition, AR also presented an anti‐inflammatory activity, as evidenced by decreased secretion of pro‐inflammatory cytokines including IL‐6, IL‐1β, and TNF‐α. Moreover, apoptotic rate was markedly decreased in HK‐2 cells pretreated with AR. The bax expression was decreased, while bcl‐2 expression was increased by AR pretreatment. Furthermore, AR enhanced the H/R‐stimulated activation of the Nrf2/HO‐1 signalling pathway in HK‐2 cells. In conclusion, these findings indicated that AR protected HK‐2 cells from H/R‐induced cell injury via regulating the Nrf2/HO‐1 signalling pathway. [ABSTRACT FROM AUTHOR]

Abstract: Recent studies have reported an important role for microRNA‐1271 (miR‐1271) in tumorigenesis. However, the role of miR‐1271 in colorectal cancer remains unknown. Here, we found that miR‐1271 was significantly decreased in colorectal cancer tissues and cell lines. Overexpression of miR‐1271 inhibited cell proliferation, colony formation, cell invasion, and induced cell cycle arrest in colorectal cancer cells. Metadherin (MTDH) was identified as a target gene of miR‐1271. Moreover, miR‐1271 negatively regulated MTDH expression in colorectal cancer cells and reversely correlated with MTDH expression in colorectal cancer specimens. Additionally, miR‐1271 also regulated the activation of Wnt signaling in colorectal cancer cells. The restoration of MTDH expression significantly reversed the antitumor effect of miR‐1271 in colorectal cancer cells. These findings indicate an important role for miR‐1271/MTDH in the tumorigenesis of colorectal cancer, and suggest that miR‐1271 may be a novel therapeutic target for colorectal cancer. [ABSTRACT FROM AUTHOR]

Rab3D is a member of the ras-related GTP-binding protein Rab family and was found up-regulated in several types of cancer. However, little is known about the role of Rab3D in carcinogenesis and progression of esophageal squamous cell carcinoma (ESCC). Thus, in this study, we investigated the expression patterns and functional roles of Rab3D in human ESCC. We demonstrated that Rab3D was highly expressed in human ESCC cell lines. In addition, knockdown of Rab3D significantly inhibited the proliferation of ESCC cells and reduced the tumorigenesis in vivo . Moreover, knockdown of Rab3D significantly suppressed ESCC cell migration/invasion and accordingly alerted EMT related markers, which including up-regulated E-cadherin and down-regulated N-cadherin in ESCC cells. Finally, knockdown of Rab3D inhibited the levels of p-PI3K and p-Akt in ECA-109 cells. In conclusion, our data demonstrated that Rab3D functions as an oncogene in ESCC and knockdown of Rab3D suppressed ESCC cell proliferation and invasion, potentially through the PI3K/Akt signaling pathway. Overall, these findings suggest that targeting the Rab3D may be a potential therapeutic target for treatment of ESCC. [ABSTRACT FROM AUTHOR]

Cancer-associated fibroblasts (CAF) play a crucial role in regulating cancer progression, yet the molecular determinant that governs the tumor regulatory role of CAF remains unknown. Using a mouse melanoma model in which exogenous melanoma cells were grafted on the skin of two lines of mice where the genetic activation or inactivation of Notch1 signaling specifically occurs in natural host stromal fibroblasts, we demonstrated that Notch1 pathway activity could determine the tumor-promoting or tumor-suppressing phenotype in CAF. CAF carrying elevated Notch1 activity significantly inhibited melanoma growth and invasion, while those with a null Notch1 promoted melanoma invasion. These findings identify the Notch1 pathway as a molecular determinant that controls the regulatory role of CAF in melanoma skin growth and invasion, unveiling Notch1 signaling as a potential therapeutic target for melanoma and potentially other solid tumors. [ABSTRACT FROM AUTHOR]

Though alprostadil has been reported to improve the impaired microcirculation of patients with pulmonary arterial hypertension, its effectiveness as a treatment for coronary microvasculature dysfunction (CMD) following ST-segment elevation myocardial infarction (STEMI) is unknown. A total of 18 miniature pigs with CMD following STEMI were randomized into three groups that received an intracoronary injection of 5 ml of normal saline, 2 mg of nicorandil or 10 µg of alprostadil immediately after measurement of the index of microcirculatory resistance (IMR) and then an intravenous drip containing 5 ml of normal saline, 2 mg of nicorandil or 10 µg of alprostadil once a day for 6 days. The IMR, cardiac function using ultrasound, infarct areas and heparanase levels in infarct areas were measured and compared between the three groups. The IMR decreased markedly 10 min after alprostadil or nicorandil intracoronary injection (both P<0.05) but not following saline injection (P>0.05). After 7 days, the IMR was substantially lower in the alprostadil and nicorandil groups compared with the saline group (both P<0.05) and the ejection fraction was considerably higher in the alprostadil and nicorandil groups compared with the saline group (both P<0.05). Differences in infarct areas and the relative heparanase expression levels among the 3 groups were similar to the differences in the ejection fraction. No significant differences in the above assessment indexes were identified in the alprostadil and nicorandil groups. Alprostadil infusion improved coronary microcirculation function, reduced the infarct area and limited left ventricular dilatation in a pig coronary microvasculature dysfunction model following STEMI. [ABSTRACT FROM AUTHOR]

In general, the biomass raw materials burned by biomass power plants generally have the characteristics of variable fuel types, high moisture content, and high volatile content. In this paper, a 130 t/h biomass circulating fluidized bed (BCFB) model was established on the MWorks platform with Modelica language. The influence of biomass type changes on operation parameters, the corresponding steady-state characteristics, and the dynamic characteristics of the BCFB were carried out. The temperature corresponding to the combustion of pine was overall higher than that of the other fuels, and the flue gas from the combustion of pine had the highest concentration of SO2, up to 520.49 mg/Nm3. The flue gas from the combustion of pure cotton sticks had the highest concentration of NO, up to 254.34 mg/Nm3. The changes of fuel type and moisture content all have a great influence on the operation of BCFBs. The emission of pollutants was not only related to the element content of fuel, but also closely related to the furnace temperature. The fuel moisture content also indirectly affects the pollutant emission concentration and the steam-water system. [ABSTRACT FROM AUTHOR]

Hyperglycemia-induced podocyte damage contributes to the onset of diabetic nephropathy, a severe complication of diabetes. Perilipin 5 (Plin5) exerts a vital role in numerous pathological conditions via affecting cell apoptosis, oxidative stress, and inflammation. However, whether Plin5 plays a role in regulating podocyte damage of diabetic nephropathy has not been fully determined. This work aimed to explore the role of Plin5 in mediating high glucose (HG)-induced injury of podocytes in vitro. Our results demonstrated that Plin5 expression was markedly decreased in mouse podocytes challenged with HG. Plin5 overexpression markedly suppressed HG-induced apoptosis, reactive oxygen species (ROS) production, and the pro-inflammatory response in podocytes. On the contrary, Plin5 silencing produced the opposite effects. Further mechanistic analysis demonstrated that Plin5 upregulation remarkably increased the levels of phospho-Akt and phospho-glycogen synthase kinase-3β (GSK-3β) in HG-exposed podocytes. Moreover, Plin5 overexpression increased the levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and enhanced the activation of Nrf2 signaling. Akt inhibition markedly blocked Plin5-mediated activation of Nrf2, while GSK-3β inhibition reversed Plin5-silencing-induced suppressive effects on Nrf2 activation. Notably, Nrf2 suppression significantly blocked Plin5-mediated protective effects against HG-induced podocyte injury. In summary, our work indicates a vital role for Plin5 in protecting against HG-induced apoptosis, oxidative stress, and inflammation in podocytes via modulation of Akt/GSK-3β/Nrf2 signaling. This study suggests that Plin5 may participate in modulating podocyte damage in diabetic nephropathy. Image 1 • Plin5 protected from HG-induced podocyte injury. • Plin5 potentiated Nrf2 signaling in HG-exposed podocytes. • Plin5 regulated Nrf2 activation by Akt/GSK-3β. • Plin5 ameliorated HG-induced podocyte injury by Nrf2. [ABSTRACT FROM AUTHOR]