Anti-Amphetamine monoclonal antibody, clone 4F32C9

A solar cell of p-i-n type, containing hydrogenated amorphous silicon (a-Si:H) is simulated using the unidimensional computer code AMPS-1D. The objective of the present contribution is to investigate the effect of the thickness of the active layer a-Si:H(i) and the variation of its density of states (DOS) on the performances of the solar cell, namely the current of short circuit (J(SC)), the tension of open circuit (V-OC), the form factor (FF) and the efficiency (E-ff). Also we aim to determine the structural parameters characterizing each layer constituting the cell. Our results show that the best thickness for the active layer that gives good performances of the studied solar cell lies between 300 and 600 nm. Besides, the best DOS that provides better output parameters of the solar cell is determined to be in the range 5.10(15)-10(16) cm(-3). After optimization, our findings give values of Voc = 1.193 V, Jsc = 13.145 mA cm(-2), FF = 0.807 which corresponds to an efficiency of E-ff = 12.655%. The optimization has been done as a function of temperature and wavelength.

As a result of the hostile microenvironment, metabolic alterations are required to enable the malignant growth of cancer cells. To understand metabolic reprogramming during metastasis, we conducted shotgun proteomic analysis of highly metastatic (HM) and non-metastatic (NM) ovarian cancer cells. The results suggest that the genes involved in fatty-acid (FA) metabolism are upregulated, with consequent increases of phospholipids with relatively short FA chains (myristic acid, MA) in HM cells. Among the upregulated proteins, ACSL1 expression could convert the lipid profile of NM cells to that similar of HM cells and make them highly aggressive. Importantly, we demonstrated that ACSL1 activates the AMP-activated protein kinase and Src pathways via protein myristoylation and finally enhances FA beta oxidation. Patient samples and tissue microarray data also suggested that omentum metastatic tumours have higher ACSL1 expression than primary tumours and a strong association with poor clinical outcome. Overall, our data reveal that ACSL1 enhances cancer metastasis by regulating FA metabolism and myristoylation.