Shc (Phospho-Tyr349) ELISA Kit

This paper presents energetic, economic, and environmental (3E) analyses of four configurations of solar heating and cooling (SHC) systems based on coupling evacuated tube collectors with a single-effect LiBr-H2O absorption chiller. In the first configuration (SHC1), a gas-fired heater is used as the back-up system, while a mechanical compression chiller is employed as the auxiliary cooling system in the second configuration (SHC2). The capacity of the absorption chiller is designed based on the maximum building cooling load in these configurations. The third and fourth configurations (SHC3 and SHC4) are similar to SHC2, but the absorption chiller size is reduced to 50% and 20%, respectively. The results show that the highest primary energy saving is achieved by SHC2, leading to a solar fraction of 71.8% and saving 54.51% primary energy as compared to a reference conventional HVAC system. The economic performance of all configurations is still unsatisfactory (without subsidies) due to their high capital costs. However, if a government subsidy of 50% is considered, the results suggest that SHC4 can be economically feasible, achieving a payback period of 4.1 years, net present value of 568,700 AUD and solar fraction of 43%, contributing to 27.16% decrease in the plant primary energy consumption. (C) 2015 Elsevier Ltd. All rights reserved.

Background and Purpose: The gp130 family of cytokines signals through receptors dimerizing with the gp130 subunit. Downstream signaling typically activates STAT3 but also SHP2/Ras/MAPK pathways. Oncostatin M (OSM) is a unique cytokine in this family since the receptor (OSMR) activates a non-redundant signaling pathway by recruitment of the adapter Shc1. We have studied the functional relevance of Shc1 for OSM-induced bone resorption. Experimental Approach: Osteoblasts were stimulated with OSM and STAT3 and Shc1 activations were studied using real-time PCR and Western blots. The role of STAT3 and Shc1 for OSM-induced RANKL expression and osteoclast formation was studied by silencing their mRNA expressions. Effects of OSM were compared to those of the closely related cytokine leukemia inhibitory factor (LIF). Key Results: OSM, but not LIF, induced the mRNA and protein expression of Shc1 and activated phosphorylation of Shc1 in the osteoblasts. Silencing of Shc1 decreased OSM-induced activation of STAT3 and RANKL expression. Silencing of STAT3 had no effect on activation of Shc1, but prevented the OSM-mediated increase of RANKL expression. Silencing of either Shc1 or STAT3 in osteoblasts decreased formation of osteoclasts in OSM-stimulated co-cultures of osteoblasts and macrophages. In agreement with these observations, OSM was a more potent and robust stimulator than LIF of RANKL formation and bone resorption in mouse calvariae and osteoclast formation in bone marrow cultures. Conclusions and Implications: Activation of the Shc1-dependent STAT3 signaling is crucial for OSM-induced osteoclast formation. Inhibition of Shc1 is a potential mechanism to specifically inhibit OSM-induced bone resorption.