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

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

Cross-corpora analysis of spatial language: The case of fictive motion

The way people describe where things are is one of the central questions of spatial information theory and has been the subject of considerable research. We investigate one particular type of location description, fictive motion (as in, The range runs along the coast). The use of this structure is known to highlight particular properties of the described entity, as well as to convey its configuration in physical space in an effective way. We annotated 496 fictive motion structures in seven corpora that represent different types of spatial discourse - news, travel blogs, texts describing outdoor pursuits and local history, as well as image and location descriptions. We analysed the results not only by examining the distribution of fictive motion structures across corpora, but also by exploring and comparing the semantic categories of verbs used in fictive motion. Our findings, first, add to our knowledge of location description strategies that go beyond prototypical locative phrases. They further reveal how the use of fictive motion varies across types of spatial discourse and reflects the nature of the described environment. Methodologically, we highlight the benefits of a cross-corpora analysis in the study of spatial language use across a variety of contexts.fals

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

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

Evaluating CPT and CPTu based pile bearing capacity estimation methods using Urmiyeh Lake Causeway piling records

AbstractUrmiyeh Lake is the largest super salt water situated in the north-west of Iran. A causeway embankment has been constructed in the narrowest part of the lake from both sides about 13.5 km, in order to connect two provincial capital cities of Tabriz and Urmiyeh of eastern and western Azerbaijan provinces to Europe through Turkey, while a 1280 m opening in between linked up by a bridge. Based on soil classification methods, utilizing CPTu data and soil sampling, the lake sediments consist of 150 m of soft and very sensitive clay. In order to evaluate the bearing capacity of driven piles of the bridge, eight long steel piles with diameters of 813 and 66 m and lengths of 75 m have been instrumented and monitored based on static and dynamic load testing program. Piezocone (CPTu) results are also available from adjacent pile locations. Results of pile capacity calculation based on direct CPT and CPTu methods demonstrate that reasonable accuracy can be achieved in reference to dynamic testing. Therefore, combination of CPTu data with dynamic testing results can be considered by engineers for predicting bearing capacity of piles in offshore and bridge structures, where the static pile load testing is difficult, time consuming and expensive in marine environment