An evaluation method of supercritical CO2 thickening result for particle transporting

This paper aims to propose an evaluation method for measuring the supercritical CO2 thickening result for particle transporting. By analyzing the particle transporting trajectory in supercritical CO2, the cotangent of particle landing angle (ratio of particle horizontal velocity to vertical velocity) was proposed as a new criterion of thickening result. Previous studies of supercritical CO2 thickening were evaluated and drawn in three dimensions using this new criterion. Moreover, the effects of CO2 density and viscosity on particle vertical and horizontal velocities and the cotangent of particle landing angle were analyzed. The cotangent of particle landing angle is more sensitive to supercritical CO2 density than viscosity. Therefore, supercritical CO2 density should be considered for the evaluation of supercritical CO2 thickening for particle transporting. The particle settling velocity was found to determine the particle transporting distance and also the transporting capability of supercritical CO2. According to this conclusion, the apparatus for experimental evaluation of supercritical CO2 thickening will be miniaturized significantly by the simplification from two-dimensional velocities measurement into one direction, particle settling velocity in vertical direction. Additionally, the supercritical CO2 viscosity was found to have an optimum value, exceeding which the effect of viscosity on particle transporting levels off

Occurrence Mechanism of Roof-Fall Accidents in Large-Section Coal Seam Roadways and Related Support Design for Bayangaole Coal Mine, China

This study focused on large-scale roof-fall accidents occurred in large-section coal seam roadways of Bayangaole Coal Mine, Inner Mongolia, China, and investigated the occurrence mechanism of roof-fall and the related supporting control method in detail. Firstly, the fracture characteristics of the surrounding rocks on the roadway roof were measured using a stratum detector. The results showed that the roadway roof underwent the most severe failure with a maximum deformation of 3.53 m; the bedding separation and fracture zones were distributed at irregular intervals. Accordingly, the entire stratum was separated into several thin sublayers, significantly reducing the stability of roof. In addition, the roof medium grained sandstone of roadway is water-rich strata, and water aggravates the damage of roof. Next, the mechanism of the occurrence of roof-fall accidents in the roadway was elucidated in detail. The following three reasons are mainly attributed to the occurrence of roof-fall accidents: (i) effects of mining-induced stress and tectonic stress, (ii) existence of equipment cavern on the side of roadway, and (iii) unreasonable support parameters. On that basis, a new supporting design is proposed, including a more reasonable arrangement of anchor cables and bolts, bolts with full-length anchorage which are applicable in cracked and water-rich roadway, high-strength anchor cables, and crisscrossed steel bands. Moreover, high pretightening force was applied. Finally, a field test was performed, and the mining-induced roof displacement and stress on anchor cable (bolt) were monitored in the test section. The maximum roof displacements at the two monitoring sections were 143 mm and 204 mm, respectively, far smaller than the roadway’s allowable deformation. Moreover, the stress on roof anchor cables (bolts) was normal, and no anchorage-dragging and tensile failure phenomena were observed. The monitoring data indicated that the new supporting design was remarkable on the control of large-section coal seam roadway roof deformation

Type I interferon/STAT1 signaling regulates UBE2M-mediated antiviral innate immunity in a negative feedback manner

Summary: Type I interferon (IFN-I) signaling is central to inducing antiviral innate immunity. However, the mechanisms for IFN-I signaling self-regulation are still largely unknown. Here, we report that RNA virus-infected macrophages with UBE2M deficiency produced decreased IFN-I expression in a RIG-I-dependent manner, causing an aggravated viral infection. Mechanistically, UBE2M inhibits RIG-I degradation by preventing the interaction of RIG-I and E3 ligase STUB1, resulting in antiviral IFN-I signaling activation. Simultaneously, IFN-I signaling-activated STAT1 facilitates the transcription of Trim21, leading to increased UBE2M degradation and blunted antiviral immunity. Translationally, oral administration of milk-derived extracellular vesicles containing RING domain-truncated TRIM21 (TRIM21-ΔRING) lacking E3 ligase activity efficiently transfers TRIM21-ΔRING into macrophages. TRIM21-ΔRING suppresses UBE2M degradation by competitively binding to UBE2M with TRIM21, thereby enhancing antiviral immunity. Overall, we reveal a negative feedback loop of IFN-I signaling and develop a reagent to improve innate immunity against RNA viruses

Role of Intratubular Pressure During the Ischemic Phase in Acute Kidney Injury

Acute kidney injury (AKI) induced by clamping of renal vein or pedicle is more severe than clamping of artery, but the mechanism has not been clarified. In the present study, we tested our hypothesis that increased proximal tubular pressure (Pt) during the ischemic phase exacerbates kidney injury and promotes the development of AKI. We induced AKI by bilateral clamping of renal arteries, pedicles, or veins for 18 min at 37°C, respectively. Pt during the ischemic phase was measured with micropuncture. We found that higher Pt was associated with more severe AKI. To determine the role of Pt during the ischemic phase on the development of AKI, we adjusted the Pt by altering renal artery pressure. We induced AKI by bilateral clamping of renal veins, and the Pt was changed by adjusting the renal artery pressure during the ischemic phase by constriction of aorta and mesenteric artery. When we decreased renal artery pressure from 85 ± 5 to 65 ± 8 mmHg, Pt decreased from 53.3 ± 2.7 to 44.7 ± 2.0 mmHg. Plasma creatinine decreased from 2.48 ± 0.23 to 1.91 ± 0.21 mg/dl at 24 h after renal ischemia. When we raised renal artery pressure to 103 ± 7 mmHg, Pt increased to 67.2 ± 5.1 mmHg. Plasma creatinine elevated to 3.17 ± 0.14 mg·dl·24 h after renal ischemia. Changes in KIM-1, NGAL, and histology were in the similar pattern as plasma creatinine. In summary, we found that higher Pt during the ischemic phase promoted the development of AKI, while lower Pt protected from kidney injury. Pt may be a potential target for treatment of AKI. acute kidney injury (AKI) is a syndrome characterized by an abrupt reduction in kidney function (1, 42), resulting in failure to maintain fluid, electrolyte and acid-base homeostasis, and retention of nitrogenous waste products (6, 30). AKI occurs in ~5% of all hospital admissions and is responsible for approximately two million deaths annually worldwide (33, 45, 46). AKI increases the risk of development of chronic kidney disease (CKD) (10, 11), exacerbates preexisting CKD, and can evolve into end-stage renal disease (ESRD) (19, 25, 48). Patients who survive an episode of AKI have poorer long-term outcomes with increased mortality and extensive morbidity (3, 23). Even though AKI is extensively studied, unfortunately, there is no approved therapy to prevent or treat AKI (20). Therefore, further understanding of the pathophysiological mechanism is crucial to develop therapeutic approaches for AKI. Renal ischemia reperfusion is a common cause of AKI (7, 24, 31). After ischemia reperfusion, tubular epithelial cells undergo serious damage, such as apical brush-border disruption, swelling, detachment from the basement membrane, and even death with acute tubular necrosis, resulting in rapid loss of kidney function (7, 13, 31). Several factors, such as hypoxia-induced ATP depletion (4, 13, 21, 28), the imbalance between superoxide (29) and nitric oxide (9, 44, 49), and the inflammatory response have been demonstrated to play important roles in renal ischemia-reperfusion injury (36, 43, 44). However, the pathophysiological mechanisms of AKI are complicated and are not well elucidated. This is especially true regarding the role of hemodynamic alterations and changes in mechanical force in the development of AKI. The commonly used AKI models induced by occlusions of renal blood flow are typically accomplished by clamping of the renal artery, pedicle (artery and vein), or vein. Previous studies have reported that renal vein or pedicle clamping produced more severe AKI than renal artery clamping alone, but the mechanism remains to be determined (22, 24, 35). In the present study, we tested our hypothesis that increased intratubular pressure of the proximal tubule (Pt) during the ischemic phase exacerbates kidney injury and promotes the development of AKI. We first measured Pt during the ischemic phase while clamping the arteries, pedicles, or veins, respectively, and found a positive correlation between the Pt and the severity of the AKI. To determine whether the Pt during the ischemic phase is a causal factor for the kidney injury, we adjusted the Pt by altering the renal artery pressure during clamping of the renal veins. We found that increasing the Pt during the ischemic phase worsens AKI while lowering the Pt protects renal function