Observation of super-Nernstian proton-coupled electron transfer and elucidation of nature of charge carriers in a multiredox conjugated polymer.

Nernstian proton-coupled electron transfer (PCET) is a fundamental process central to many physical and biological systems, such as electrocatalysis, enzyme operation, DNA biosynthesis, pH-/bio-sensors, and electrochemical energy storage devices. We report herein the discovery of super-Nernstian PCET behavior with two protons per electron transferred in the electrochemical doping of a redox conjugated polymer, phenazine-substituted ladder poly(benzimidazobenzophenanthroline) (BBL-P), in aqueous electrolyte. We show that the super-Nernstian response originates from existence of multiredox centers that have a gradient of pKa on the conjugated polymer. Our use of various pH-dependent in operando techniques to probe the nature of charge carriers in n-doped BBL-P found that polarons are the charge carriers at low to intermediate levels of doping (0.1-1.0 electron per repeat unit (eru)) whereas at higher doing levels (1.3 eru), polarons, polaron pairs, and bipolarons co-exist, which evolve into strongly coupled polaron pairs at the highest doping levels (>1.5 eru). We show that PCET-assisted n-doping of BBL-P results in very high redox capacity (>1200 F cm-3) in acidic electrolyte. Our results provide important new insights into PCET in organic materials and the nature of charge carriers in n-doped conjugated polymers while having implications for various electrochemical devices.

Chain Length Dependence of Electron Transport in an n-Type Conjugated Polymer with a Rigid-Rod Chain Topology.

Most currently known n-type conjugated polymers have a semiflexible chain topology, and their charge carrier mobilities are known to peak at modest chain lengths of below 40-60 repeat units. Herein, we show that the field-effect electron mobility of a model n-type conjugated polymer that has a rigid-rod chain topology grows continuously without saturation, even at a chain length exceeding 250 repeat units. We found the mechanism underlying the novel chain length-dependent electron transport to originate from the reduced structural disorder and energetic disorder with the increasing degree of polymerization inherent to the rigid-rod chain topology. Furthermore, we demonstrate a unique chain length-dependent decay of threshold voltage, which is rationalized by decreased trap densities and trap depths with respect to the degree of polymerization. Our findings provide new insights into the role of polymer chain topology in electron transport and demonstrate the promise of rigid-rod chain architectures for the design of future high-mobility conjugated polymers.

Interaction of pre- and postnatal nutrition on expression of leptin receptor variants and transporter molecules, leptin transport, and functional response to leptin in heifers†.

Perinatal nutrition modulates the hypothalamic neurocircuitries controlling GnRH release, thus programming pubertal maturation in female mammals. Objectives of experiments reported here were to test the hypotheses that prenatal nutrition during mid- to late gestation interacts with postnatal nutrition during the juvenile period in heifer offspring to alter expression of leptin receptor (LepR) variants (ObRa, ObRb, ObRc, ObRt), and lipoprotein transporter molecules (LRP1 and 2) in the choroid plexus, leptin transport across the blood-brain barrier, and hypothalamic-hypophyseal responsiveness to exogenous ovine leptin (oleptin) during fasting. Nutritional programming of heifers employed a 3 × 2 factorial design of maternal (high, H; low, L; and moderate, M) × postnatal (H and L) dietary treatments. Results (Expt. 1) demonstrated that prepubertal heifers born to L dams, regardless of postnatal diet, had reduced expression of the short isoform of ObRc compared to H and M dams, with sporadic effects of undernutrition (L or LL) on ObRb, ObRt, and LRP1. Intravenous administration of oleptin to a selected postpubertal group (HH, MH, LL) of ovariectomized, estradiol-implanted heifers fasted for 56 h (Expt. 2) did not create detectable increases in third ventricle cerebrospinal fluid but increased gonadotropin secretion in all nutritional groups tested. Previous work has shown that leptin enhances gonadotropin secretion during fasting via effects at both hypothalamic and anterior pituitary levels in cattle. Given the apparent lack of robust transfer of leptin across the blood-brain barrier in the current study, effects of leptin at the adenohypophyseal level may predominate in this experimental model.

Review: Gestational and postnatal nutritional effects on the neuroendocrine control of puberty and subsequent reproductive performance in heifers.

Pubertal attainment is an intricate biological process that involves maturation of the reproductive neuroendocrine axis and increased pulsatile release of gonadotropin-releasing hormone (GnRH) and luteinizing hormone. Nutrition is a critical environmental factor controlling the timing of puberty attainment. Nutrient restriction during early postnatal development delays puberty, whereas increased feed intake and adiposity during this period hasten pubertal maturation by imprinting the hypothalamus. Moreover, the dam's nutrition during gestation can program the neuroendocrine system in the developing fetus and has the potential to advance or delay puberty in the offspring. Leptin, a hormone produced primarily by adipose cells, plays an important role in communicating energy status to the brain and regulating sexual maturation. Leptin's regulation of GnRH release is mediated by an upstream neuronal network since GnRH neurons do not contain the leptin receptor. Two groups of neurons located in the arcuate nucleus of the hypothalamus that express neuropeptide Y (NPY), an orexigenic peptide, and alpha melanocyte-stimulating hormone (αMSH), an anorexigenic peptide, are central elements of the neural circuitry that relay inhibitory (NPY) and excitatory (αMSH) inputs to GnRH neurons. Moreover, KNDy neurons, neurons in the arcuate nucleus that co-express kisspeptin, neurokinin B (NKB), and dynorphin, also play a role in the metabolic regulation of puberty. Our studies in beef heifers demonstrate that increased rates of BW gain during early postweaning (4-9 mo of age) result in reduced expression of NPY mRNA, increased expression of proopiomelanocortin and kisspeptin receptor mRNA, reduced NPY inhibitory inputs to GnRH neurons, and increased excitatory αMSH inputs to KNDy neurons. Finally, our most recent data demonstrate that nutrition of the cow during the last two trimesters of gestation can also induce transcriptional and structural changes in hypothalamic neurocircuitries in the heifer progeny that likely persist long-term after birth. Managerial approaches, such as supplementation of the dam during gestation (fetal programming), creep feeding, early weaning, and stair-step nutritional regimens have been developed to exploit brain plasticity and advance pubertal maturation in heifers.