Polycyclic Aromatic Hydrocarbons Concentration in Straw Biochar with different Particle Size

AbstractBiochar, a carbon-rich material formed by a biomass pyrolyzed at relatively low temperatures (≤700°C), showed attractive sorption capacity on both organic pollutants and heavy metals and wildly used in various areas of environmental engineering. However, polycyclic aromatic hydrocarbons (PAHs) may also be assumed to be produced for the oxygen-limited pyrolysis condition in biochar production process. It is not well known about the affect of particle size in concentration and distributing characteristic of PAHs of biochar. In the current study, twenty-seven PAHs concentration in maize straw biochar produced with different powder particle size (9.31, 20.26, 60.77, 71.07, 101.9μm) were quantified, and the ∑27PAHs, total LMW PAHs, total MMW PAHs and total HMW PAHs concentration were analyzed. As the particle size increase, the ∑27PAHs concentrations show a trend of firstly increase and then decrease, and the maximum appears at 60.77μm (166.52 ng/g) and the minimum appears at 101.90μm (14.63 ng/g). LMW total PAHs and total MMW PAHs concentrations firstly increase and then decrease, with the particle size increasing from 9.31μm to 101.9μm. Meanwhile, the total HMW PAH concentrations decrease gradually when biochar particle size increasing. Compared to US, UK background soil concentrations and Canada standards, it is appropriate to conclude that PAHs in straw biochar have minimal effects after application to soil especially at 101.9μm

Genetic Deletion of KLHL1 Leads to Hyperexcitability in Hypothalamic POMC Neurons and Lack of Electrical Responses to Leptin

Kelch-like 1 (KLHL1) is a neuronal actin-binding protein that modulates voltage-gated calcium channels. The KLHL1 knockout (KO) model displays altered calcium channel expression in various brain regions. We analyzed the electrical behavior of hypothalamic POMC (proopiomelanocortin) neurons and their response to leptin. Leptin’s effects on POMC neurons include enhanced gene expression, activation of the ERK1/2 pathway and increased electrical excitability. The latter is initiated by activation of the Jak2-PI3K-PLC pathway, which activates TRPC1/5 (Transient Receptor Potential Cation) channels that in turn recruit T-type channel activity resulting in increased excitability. Here we report over-expression of CaV3.1 T-type channels in the hypothalamus of KLHL1 KO mice increased T-type current density and enhanced POMC neuron basal excitability, rendering them electrically unresponsive to leptin. Electrical sensitivity to leptin was restored by partial blockade of T-type channels. The overexpression of hypothalamic T-type channels in POMC neurons may partially contribute to the obese and abnormal feeding phenotypes observed in KLHL1 KO mice.Fil: Perissinotti, Paula Patricia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; ArgentinaFil: Martínez Hernández, Elizabeth. Loyola University Of Chicago; Estados UnidosFil: He, Yungui. University of Minnesota; Estados UnidosFil: Koob, Michael D.. University of Minnesota; Estados UnidosFil: Piedras Rentería, Erika S.. Loyola University Of Chicago; Estados Unido

Constraining the interacting dark energy models from weak gravity conjecture and recent observations

We examine the effectiveness of the weak gravity conjecture in constraining the dark energy by comparing with observations. For general dark energy models with plausible phenomenological interactions between dark sectors, we find that although the weak gravity conjecture can constrain the dark energy, the constraint is looser than that from the observations.Comment: 14 pages, 12 figures, revtex4, v2: minor corrections, accepted for publication in PL

KLHL1 Controls CaV3.2 Expression in DRG Neurons and Mechanical Sensitivity to Pain

Dorsal root ganglion (DRG) neurons process pain signaling through specialized nociceptors located in their peripheral endings. It has long been established low voltage-activated (LVA) CaV3.2 calcium channels control neuronal excitability during sensory perception in these neurons. Silencing CaV3.2 activity with antisense RNA or genetic ablation results in anti-nociceptive, anti-hyperalgesic and anti-allodynic effects. CaV3.2 channels are regulated by many proteins (Weiss and Zamponi, 2017), including KLHL1, a neuronal actin-binding protein that stabilizes channel activity by recycling it back to the plasma membrane through the recycling endosome. We explored whether manipulation of KLHL1 levels and thereby function as a CaV3.2 modifier can modulate DRG excitability and mechanical pain transmission or sensitivity to pain. We first assessed the mechanical sensitivity threshold and DRG properties in the KLHL1 KO mouse model. KO DRG neurons exhibited smaller T-type current density compared to WT without significant changes in voltage dependence, as expected in the absence of its modulator. Western blot analysis confirmed CaV3.2 but not CaV3.1, CaV3.3, CaV2.1, or CaV2.2 protein levels were significantly decreased; and reduced neuron excitability and decreased pain sensitivity were also found in the KLHL1 KO model. Analogously, transient down-regulation of KLHL1 levels in WT mice with viral delivery of anti-KLHL1 shRNA also resulted in decreased pain sensitivity. These two experimental approaches confirm KLHL1 as a physiological modulator of excitability and pain sensitivity, providing a novel target to control peripheral pain.Fil: Martínez Hernández, Elizabeth. Loyola University Chicago; Estados UnidosFil: Zeglin, Alissa. Loyola University Chicago; Estados UnidosFil: Almazan, Erik. Loyola University Chicago; Estados UnidosFil: Perissinotti, Paula Patricia. Loyola University Chicago; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; ArgentinaFil: He, Yungui. University of Minnesota; Estados UnidosFil: Koob, Michael. University of Minnesota; Estados UnidosFil: Martin, Jody L.. Loyola University Chicago; Estados UnidosFil: Piedras-Rentería, Erika S.. Loyola University Chicago; Estados Unido