Anti-AMH (C-terminal) polyclonal antibody

Amorphous metal hydroxides (AMHs) of earth-abundant transition metal elements (Fe, Co and Ni) have emerged as promising electrocatalysts for developing clean energy and conversion, especially toward the anode oxygen evolution reaction (OER), owing to their low cost, high conductivity and amorphous structures. Here, as a proof-of-concept experiment, a rapid one-step and very effective synthesis strategy is reported for the first time to produce a family of ionic liquid-modified AMH nanoparticles as highly efficient OER electrocatalysts. The ionic liquid-modified bimetallic FeNi hydroxide nanoparticles exhibit remarkable OER activity with a Tafel slope of 54.4 mV dec(-1)and an overpotential of 300 mV for 10 mA cm(-2)(loading: similar to 0.009 mg(FeNi)cm(-2)). Further, the universal applicability of this strategy for designing the AMH nanoparticles extends to other metallic hydroxide nanoparticles (Fe, Co, Ni, FeCo and NiCo). This work may provide a novel synthetic protocol to design amorphous metal hydroxide nanoparticle catalysts for the efficient OER.

Background The increasing incidence of reproductive disorders in humans has been attributed to in utero exposure to estrogenic endocrine disruptors. In particular, exposure of the developing testis to exogenous estrogen can negatively impact male reproductive health. To determine how estrogens impact human gonad function, we treated the human testis-derived cell line NT2/D1 with estrogen and examined its impact on SOX9 and the expression of key markers of granulosa (ovarian) and Sertoli (testicular) cell development. Results Estrogen successfully activated its cognate receptor (estrogen receptor alpha;ESR1) in NT2/D1 cells. We observed a significant increase in cytoplasmic SOX9 following estrogen treatment. After 48 h of estrogen exposure, mRNA levels of the key Sertoli cell genesSOX9, SRY, AMH, FGF9andPTGDSwere significantly reduced. This was followed by a significant increase in mRNA levels for the key granulosa cell genesFOXL2andWNT4after 96 h of estrogen exposure. Conclusions These results are consistent with estrogen's effects on marsupial gonads and show that estrogen has a highly conserved impact on gonadal cell fate decisions that has existed in mammals for over 160 million years. This effect of estrogen presents as a potential mechanism contributing to the significant decrease in male fertility and reproductive health reported over recent decades. Given our widespread exposure to estrogenic endocrine disruptors, their effects on SOX9 and Sertoli cell determination could have considerable impact on the adult testis.