Evaluation of the effect of sodium silicate addition to mine backfill, Gelfill − Part 1

In this paper, the mechanical properties of sodium silicate-fortified backfill, called Gelfill, were investigated by conducting a series of laboratory experiments. Two configurations were tested, i.e. Gelfill and cemented hydraulic fill (CHF). The Gelfill has an alkali activator such as sodium silicate in its materials in addition to primary materials of mine backfill which are tailings, water and binders. Large numbers of samples of Gelfill and CHF with various mixture designs were cast and cured for over 28 d. The mechanical properties of samples were investigated using uniaxial compression test, and the results were compared with those of reference samples made without sodium silicate. The test results indicated that the addition of an appropriate amount of an alkali activator such as sodium silicate can enhance the mechanical (uniaxial compressive strength) and physical (water retention) properties of backfill. The microstructure analysis conducted by mercury intrusion porosimetry (MIP) revealed that the addition of sodium silicate can modify the pore size distribution and total porosity of Gelfill, which can contribute to the better mechanical properties of Gelfill. It was also shown that the time and rate of drainage in the Gelfill specimens are less than those in CHF specimens made without sodium silicate. Finally, the study showed that the addition of sodium silicate can reduce the required setting time of mine backfill, which can contribute to increase mine production in accordance with the mine safety

Evaluation of the effect of sodium silicate addition to mine backfill, Gelfill – Part 2: Effects of mixing time and curing temperature

The effects of mixing time and curing temperature on the uniaxial compressive strength (UCS) and microstructure of cemented hydraulic fill (CHF) and sodium silicate-fortified backfill (Gelfill) were investigated in the laboratory. A series of CHF and Gelfill samples was mixed for time periods ranging from 5 min to 60 min and cured at temperatures ranging from 5 �Cto 50 �C for 7 d, 14 d or 28 d. Increasing the mixing time negatively influenced the UCS of Gelfill samples, but did not have a detectable effect on CHF samples. The curing temperature had a strong positive impact on the UCSs of both Gelfill and CHF. An elevated temperature caused rapid UCS development over the first 14 d of curing. Mercury intrusion porosimetry (MIP) indicated that the pore size distribution and total porosity of Gelfill were altered by curing temperature

2.20 Behcet’s disease and miscellaneous rheumatic conditions

Background: Behcet’s disease is an inflammatory, systemic and chronic disorder with unknown etiology affecting multiple systems of body (1). The cause is not clear but seems to be multifactorial, including immune system dysfunction (humoral and cellular immune defects), endothelial cell dysfunction and genetic predisposition (2). White adipose tissue produces variety of proteins in the name of adipocytokines, with important roles in body metabolism. One of these newly identified secreted adipocytokines is visfatin, which is secreted by the visceral fat and its plasma level increases during the obesity. It has insulinmimetic effects in metabolism of cultured cells and activates the insulin receptor (3). Visfatin stimulates inflammatory cells like monocytes and can induces increasing circulating level of IL-6 in mice. It have been considered as a new proinflammatory adipocytokine (4). Previous studies have evaluated visfatin level in immunologic disorders like rheumatoid arthritis and showed it was significantly higher in comparing to control subjects (4,5,6). There was no evaluation in patients with behcet disease yet. Objectives: We have evaluated visfatin level in patients with behcet disease finding inflammatory role of that in pathogenesis and clinical manifestations of behcet disease. Methods: We have evaluated 40 patients with Behcet’s disease fulfilled the International Study Group Criteria for the Diagnosis of Behc¸et’s Disease (ISG) and 40 healthy subjects from healthy candidates referring to behcet clinic of Shiraz medical university as a referral center for these patients in south Iran. Both groups have been matched for age, body mass index (BMI) and sex. Visfatin was checked in both groups using ELISA Kit. Results: There were no significant difference between cases and controls in mean concentration of visfatin level (P = 0.61). Difference in the visfatin level between patients with active and inactive manifestations of Behcet’s disease approximated to the significant levels (6.13 3.20 and 4.25 2.73, respectively; P = 0.07). Conclusion: In view of our study, we have concluded that visfatin levels may affect the clinical manifestations of BD maybe as a proinfalmmatory marker in pathogenesis and active manifestations of Behcet’s disease although more cases should be included in future works

Determination of serum visfatin level in patients with Behcet disease, comparing with normal population

Background: Behcet’s disease is an inflammatory, systemic and chronic disorder with unknown etiology affecting multiple systems of body (1). The cause is not clear but seems to be multifactorial, including immune system dysfunction (humoral and cellular immune defects), endothelial cell dysfunction and genetic predisposition (2). White adipose tissue produces variety of proteins in the name of adipocytokines, with important roles in body metabolism. One of these newly identified secreted adipocytokines is visfatin, which is secreted by the visceral fat and its plasma level increases during the obesity. It has insulinmimetic effects in metabolism of cultured cells and activates the insulin receptor (3). Visfatin stimulates inflammatory cells like monocytes and can induces increasing circulating level of IL-6 in mice. It have been considered as a new proinflammatory adipocytokine (4). Previous studies have evaluated visfatin level in immunologic disorders like rheumatoid arthritis and showed it was significantly higher in comparing to control subjects (4,5,6). There was no evaluation in patients with behcet disease yet. Objectives: We have evaluated visfatin level in patients with behcet disease finding inflammatory role of that in pathogenesis and clinical manifestations of behcet disease. Methods: We have evaluated 40 patients with Behcet’s disease fulfilled the International Study Group Criteria for the Diagnosis of Behc¸et’s Disease (ISG) and 40 healthy subjects from healthy candidates referring to behcet clinic of Shiraz medical university as a referral center for these patients in south Iran. Both groups have been matched for age, body mass index (BMI) and sex. Visfatin was checked in both groups using ELISA Kit. Results: There were no significant difference between cases and controls in mean concentration of visfatin level (P = 0.61). Difference in the visfatin level between patients with active and inactive manifestations of Behcet’s disease approximated to the significant levels (6.13 3.20 and 4.25 2.73, respectively; P = 0.07). Conclusion: In view of our study, we have concluded that visfatin levels may affect the clinical manifestations of BD maybe as a proinfalmmatory marker in pathogenesis and active manifestations of Behcet’s disease although more cases should be included in future works

Impaired Rho GTPase activation abrogates cell polarization and migration in macrophages with defective lipolysis

Infiltration of monocytes and macrophages into the site of inflammation is critical in the progression of inflammatory diseases such as atherosclerosis. Cell migration is dependent on the continuous organization of the actin cytoskeleton, which is regulated by members of the small Rho GTPase family (RhoA, Cdc42, Rac) that are also important for the regulation of signal transduction pathways. We have recently reported on reduced plaque formation in an atherosclerotic mouse model transplanted with bone marrow from adipose triglyceride lipase-deficient (Atgl−/−) mice. Here we provide evidence that defective lipolysis in macrophages lacking ATGL, the major enzyme responsible for triacylglycerol hydrolysis, favors an anti-inflammatory M2-like macrophage phenotype. Our data implicate an as yet unrecognized principle that insufficient lipolysis influences macrophage polarization and actin polymerization, resulting in impaired macrophage migration. Sustained phosphorylation of focal adhesion kinase [due to inactivation of its phosphatase by elevated levels of reactive oxygen species (ROS)] results in defective Cdc42, Rac1 and RhoA activation and in increased and sustained activation of Rac2. Inhibition of ROS production restores the migratory capacity of Atgl−/− macrophages. Since monocyte and macrophage migration are a prerequisite for infiltrating the arterial wall, our results provide a molecular link between lipolysis and the development of atherosclerosis

C16 ceramide is crucial for triacylglycerol-induced apoptosis in macrophages

Triacylglycerol (TG) accumulation caused by adipose triglyceride lipase (ATGL) deficiency or very low-density lipoprotein (VLDL) loading of wild-type (Wt) macrophages results in mitochondrial-mediated apoptosis. This phenotype is correlated to depletion of Ca2+ from the endoplasmic reticulum (ER), an event known to induce the unfolded protein response (UPR). Here, we show that ER stress in TG-rich macrophages activates the UPR, resulting in increased abundance of the chaperone GRP78/BiP, the induction of pancreatic ER kinase-like ER kinase, phosphorylation and activation of eukaryotic translation initiation factor 2A, the translocation of activating transcription factor (ATF)4 and ATF6 to the nucleus and the induction of the cell death executor CCAAT/enhancer-binding protein homologous protein. C16:0 ceramide concentrations were increased in Atgl–/– and VLDL-loaded Wt macrophages. Overexpression of ceramide synthases was sufficient to induce mitochondrial apoptosis in Wt macrophages. In accordance, inhibition of ceramide synthases in Atgl–/– macrophages by fumonisin B1 (FB1) resulted in specific inhibition of C16:0 ceramide, whereas intracellular TG concentrations remained high. Although the UPR was still activated in Atgl–/– macrophages, FB1 treatment rescued Atgl–/– macrophages from mitochondrial dysfunction and programmed cell death. We conclude that C16:0 ceramide elicits apoptosis in Atgl–/– macrophages by activation of the mitochondrial apoptosis pathway

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

Calcium and Phosphorus metabolism during Methylprednisolone puls therapy

Abstract: Intravenous glucocorticoid pulse therapy is a common treatment for immunologically origin diseases but it can not be considered a completely benign treatment. The effects of long term administration of glucocorticoids on calcium and phosphorus metabolism are well known, but less is known a bout the effect of pulse therapy. The purpose of this study was to investigate the effect of methylprednisolone pulse therapy on serum and urinary calcium and phosphorus and serum parathormone. In this prospective study 40 patients who received methylprednisolone pulse therapy for different reasons were investigated. Patients with renal insufficiency and those taking medications affecting calcium and phosphorus metabolism were excluded. Serum calcium, phosphorus, parathormone, creatinine and urinary calcium, phosphorus, and creatinine were measured before pulse therapy and in three consecutive days after treatment. This intervention had no effect on serum calcium, parathormone and urinary calcium. Serum phosphorus decreased with a nadir on the second day and urinary phosphorus increased. It was concluded that glucocorticoid pulse therapy directly increases renal phosphorus excretion, but calcium metabolism is not disturbed. Keywords: Glucocorticoid, Methylprednisolone puls therapy, Calcium, Phophorus, Parathormo