Human, Rat, Mouse Neurotensin ELISA Kit

Bi/Bi2MoO6/TiO2 NTs photocatalysts were synthesized on the basis of TiO2 NTs by a solvothermal method using glucose as the reducing agent. The removal of organic dyes such as RhB and MB and heavy metal ions like Cr(VI) were used to simulate industrial wastewater for the photocatalytic activity assessment of Bi/Bi2MoO6/TiO2 NTs. Na2S/Na2SO3 solution was used as sacrificial agent to study the photocatalytic hydrogen generation performance of samples. The results showed that Bi3+ was successfully reduced to metal Bi and deposited on the surface of Bi2MoO6. The removal efficiencies of RhB, MB and Cr(VI) reached 73.21%, 92.98% and 70.54%, respectively, which confirmed the excellent photocatalytic activity of samples. The photocatalytic hydrogen production performance of the sample was also remarkable and the hydrogen generation rate reached 173.41 mol.h(-1).cm(-2). The active species and photocatalytic mechanism of pollutant degradation and hydrogen generation were proposed based on the photoelectrochemical data. The excellent photocatalytic performances of Bi/Bi2MoO6/TiO2 NTs will exhibit prospective guidance for the preparation and photocatalytic water splitting of bismuth-based photocatalysts.

The cytokine, GDF15, is produced in pathological states which cause cellular stress, including cancer. When over expressed, it causes dramatic weight reduction, suggesting a role in disease-related anorexia. Here, we demonstrate that the GDF15 receptor, GFRAL, is located in a subset of cholecystokinin neurons which span the area postrema and the nucleus of the tractus solitarius of the mouse. GDF15 activates GFRAL(AP/NTS) neurons and supports conditioned taste and place aversions, while the anorexia it causes can be blocked by a monoclonal antibody directed at GFRAL or by disrupting CCK neuronal signalling. The cancer-therapeutic drug, cisplatin, induces the release of GDF15 and activates GFRAL(AP/NTS) neurons, as well as causing significant reductions in food intake and body weight in mice. These metabolic effects of cisplatin are abolished by pretreatment with the GFRAL monoclonal antibody. Our results suggest that GFRAL neutralising antibodies or antagonists may provide a co-treatment opportunity for patients undergoing chemotherapy.