93 research outputs found
The dataset describes: HIF-1 α expression and LPS mediated cytokine production in MKP-1 deficient bone marrow derived murine macrophages
No full textThe data presented in this article are related to the research article entitled “MKP-1 negatively regulates LPS-mediated IL-1β production through p38 activation and HIF-1α expression” (Talwar et al., 2017) [1]. This data describes that LPS-mediated p38 and JNK phosphorylation is enhanced in MKP-1 deficient macrophages. HIF-1α expression and its nuclear accumulation are significantly increased in the nuclear extracts of MKP-1 deficient BMDMs. MKP-1 deficient BMDMs exhibited higher expression of the coactivator p300 of HIF-1α both at baseline and after LPS challenge. Inhibition of p38 MAP kinase decreased LPS mediated HIF-1α protein levels and its nuclear translocation in MKP-1 deficient BMDMs. Inhibition of p38 MAP kinase inhibited LPS induced pro-inflammatory cytokines including IL-1β, IL-6 and TNF-α
p38γ Activation and BGP (Biliary Glycoprotein) Induction in Primates at Risk for Inflammatory Bowel Disease and Colorectal Cancer—A Comparative Study with Humans
No full textColorectal cancer (CRC) is a common cause of cancer-related deaths largely due to CRC liver metastasis (CRLM). Identification of targetable mechanisms continues and includes investigations into the role of inflammatory pathways. Of interest, MAPK is aberrantly expressed in CRC patients, yet the activation status is not defined. The present study assessed p38γ activation in CRC patients, cancer cells, and tissues of cotton top tamarin (CTT) and common marmoset (CM). The primate world is an overlooked resource as colitis-CRC-prone CTT are usually inure to liver metastasis while CM develop colitis but not CRC. The results demonstrate that p38γ protein and phosphorylation levels are significantly increased in CRC patients compared to normal subjects and CTT. Furthermore, p38γ phosphorylation is significantly elevated in human CRC cells and hepatoblastoma cells but not in CM colon. Additionally, carcinoembryonic antigen (CEA) and biliary glycoprotein (BGP) are induced in the CRC patients that showed p38γ phosphorylation. Inhibition of p38 MAPK in CRC cells showed a significant decline in cell growth with no effect on apoptosis or BGP level. Overall, p38γ is activated in CRC tumorigenesis and likely involves CEA antigens during CRLM in humans but not in the CTT or CM, that rarely develop CRLM
Operational strategies for HVDC transmission in smart grids: the security versus markets dilemma
No full textOver the last decades, the European transmission system has made many profound changes in the network and has focused on three main concepts: i) flexibility, ii) integration, and iii) sustainability to increase the technological innovations, and to improve the market design. The currently used methodby transmission system operators (TSOs) is trying to accomplish these requirements, but it is important to realize that each TSO has its own grid protocols and standards. Consequently, all major TSOs in the interconnected meshed European transmission system are facing a huge difficulty in maintaining a strong operational coordination to work together as a one single European technical market model. In order to guarantee the highest security of electricity supply, it is necessary to structure a stable, reliable and secure analytical AC framework that takes into consideration the stochastic nature of system in-feeds in the daily operational planning. In this thesis it is analyzed how incorporation of smart technologies such as HVDC transmission can be used as a smart grid solution to improve the power system security and lower the risk in different adjacent areas/zones. The proposed risk-based security assessment (RBSA) methodology based on Monte-Carlo sampling is employed to investigate the security of the system and to quantify the expected system risk. It is shown that the market optimal HVDC power set-points may result in unnecessarily high risk when subjected to the unavoidable uncertainty of inputs(fluctuations in load and RES) inherent to day-ahead forecasting. A detailed comparison of market optimal versus security optimal HVDC power set-point is presented. It is proposed to properly adapt the HVDC set-points with respect to the actual operating situation, which can be quite different from the day-ahead point forecast. Moreover, it is shown that by being able to adapt HVDC set-points in realtime operation, further more serious and more costly remedial actions such as active re-dispatch and load shedding, can be avoided. Furthermore, a study with two HVDC transmission lines is performed to show the necessity of coordinated control of the HVDC lines, and how this can reduce the stress in the network by acting as a tool to shift generation.Electrical Engineering | Sustainable Energy Technolog
Evidence for a GTP-binding protein coupling thrombin receptor to PIP2-phospholipase C in membranes of hamster fibroblasts
No full textAbstractTwo different methods were used to study directly α-thrombin modulation of polyphosphoinositide breakdown in membranes prepared from Chinese hamster lung (CHL) fibroblasts. In the first one we labelled the lipid pool by incubating the intact cells with myo-[su3H]inositol prior to membrane isolation; in the other we used exogenous [3H]PIP2 with phosphatidylethanolamine (1:10) added as liposomes to freshly isolated membranes. A Ca2+-dependent PIP2 and PIP phospholipase C activity was characterized by measuring the rate of formation of inositol tris- and bisphosphate. Basal phospholipase C activity was stimulated up to 3-fold by GTP or GTP-γ-S. Of the two mitogens, α-thrombin and EGF, known to stimulate DNA synthesis in Chinese hamster fibroblasts, only α-thrombin is a potent activator of PIP2 breakdown in intact cells. Consistent with this observation, α-thrombin but not EGF potentiated GTP-γ-S-dependent phospholipase C activity in membrane preparations. These results strongly support the hypothesis that a GTP-binding protein couples α-thrombin receptor to PIP2 hydrolysis. Because both methods used to assay phospholipase C gave identical results, we conclude that the coupling is at the level of PIP2-phosphodiesterase activity
The dataset describes: HIF-1 α expression and LPS mediated cytokine production in MKP-1 deficient bone marrow derived murine macrophages
No full textBradykinin Induces Phosphoinositide Turnover, 1,2-Diglyceride Formation, and Growth in Cultured Adult Human Keratinocytes
No full textThe effects of bradykinin on activation of phosphoinositide turnover, 1 ,2-diglyceride formation, and growth of cultured adult human keratinocytes were investigated. Keratinocytes specifically bound [3H]bradykinin with high affinity (kd = 3,4 nM) and displayed 1.5×105 binding sites/cell. Bradykinin caused a rapid dose-dependent increase in inositol trisphosphate (IP3) inositol bisphosphate, and inositol monophosphate. IP3 was maximally increased (fivefold) at 30s and remained elevated for at least 10 min. Half maximal stimulation of IP3 formation was observed at 27 nM bradykinin. IP3 accumulation was equally elevated by bradykinin and lys-bradykinin but was not stimulated by des-Arg9-bradykinin, indicating that phospholipase C in cultured keratinocytes is coupled to B2 bradykinin receptors. Treatment of keratinocytes with active phorbol ester (TPA) caused a significant inhibition (50%) of bradykinin-induced IP3 accumulation, suggesting negative regulation of phospholipase C by protein kinase C. Bradykinin also caused a significant elevation in 1,2-diacylglycerol (DAG) content. DAG content was maximally elevated (twofold) at 1 min and remained elevated for at least 10 min% Bradykinin also caused a significant (two-fold, p < 0.02) increase in keratinocyte growth. These data demonstrate that bradykinin is a potent agonist of the phospholipase C/protein kinase C signal transduction system in cultured adult human keratinocytes and that activation of this pathway by bradykinin is associated with increased keratinocyte growth
Bradykinin Induces Phosphoinositide Turnover, 1,2-Diglyceride Formation, and Growth in Cultured Adult Human Keratinocytes
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