Simultaneous treatment of phosphorus and fluoride wastewater using acid-modified iron-loaded electrode capacitive deionization: Preparation and performance

Here, capacitive deionization technology (CDI) using modified activated carbon fiber felt (ACF) electrodes was proposed to provide a new strategy for the challenge of simultaneous phosphorus and fluoride wastewater treatment. The acid-modified iron-loaded ACF (A@Fe-ACF) was obtained by modifying ACF through a two-step impregnation method. After the modification, the oxygen-containing functional groups on ACF increased and provided more adsorption sites. The electron transfer efficiency on the A@Fe-ACF was increased by introducing Fe and synergistically promoted the adsorption of phosphorus and fluorine. Results showed that the removal efficiencies of total phosphorus (TP) and total fluorine (TF) in wastewater reached 89.4% and 85% under optimal conditions (voltage intensity 1.5 V, pH 7, plate spacing 1 cm), while the adsorption mechanism of phosphorus and fluorine was dominated by chemical adsorption. Meanwhile, A@Fe-ACF electrode has good recyclability and stability after five cycles

Less Conserved LRRs Is Important for BRI1 Folding

Brassinosteroid insensitive 1 (BRI1) is a multidomain plant leucine-rich repeat receptor-like kinase (LRR-RLK), belongs to the LRR X subfamily. BRI1 perceives plant hormone brassinosteroids (BRs) through its extracellular domain that constitutes of LRRs interrupted by a 70 amino acid residue island domain (ID), which activates the kinase domain (KD) in its intracellular domain to trigger BR response. Thus, the KD and the ID of BRI1 are highly conserved and greatly contribute to BR functions. In fact, most bri1 mutants are clustered in or surrounded around the ID and the KD. However, the role of the less conserved LRR domains, particularly the first few LRRs after the signal peptide, is elusive. Here, we report the identification of a loss-of-function mutant bri1-235 that carries a mutation in the less conserved fourth LRR of BRI1 extracellular domain in Arabidopsis. This mutant had a base alteration from C to T, resulting in an amino acid substitution from serine to phenylalanine at the 156th position of BRI1. Compared with the wild-type plants, bri1-235 exhibited round leaves, prolonged life span, shorter stature, and approximately normal fertility under light conditions. The bri1-235 mutant was less sensitive to exogenous brassinolide under normal conditions. Importantly, both wild-type BRI1 expression and a sbi1 mutant that activates BRI1 rescued bri1-235 and resembled the wild type. Furthermore, bri1-235 protein was localized in endoplasmic reticulum rather than plasma membrane, suggestive of a cause for reducing BR sensitive in bri1-235. Taken together, our findings provide an insight into the role of the less conserved LRRs of BRI1, shedding light on the role of LRRs in a variety of LRR-RLKs that control numerous processes of plant growth, development, and stress response

Functional trait data for vascular plant species from eastern North America

Wisconsin’s plant communities are responding to shifting disturbance regimes, habitat fragmentation, aerial nitrogen deposition, exotic species invasions, ungulate herbivory, and successional processes. To better understand how plant functional traits mediate species’ responses to environmental conditions, we collected a large set of functional trait data for vascular plant species occupying Wisconsin forests and grasslands. We used standard protocols to make 76,213 measurements of 34 quantitative traits. These data provide rich information on genome size, physical leaf traits (length, width, circularity, thickness, dry matter content, specific leaf area, etc.), chemical leaf traits (carbon, nitrogen, phosphorus, potassium, calcium, magnesium, ash), life history traits (vegetative and flower heights, seed mass), and traits affecting plant palatability (leaf fiber, fat, and lignin). These trait values derive from replicate measurements on 12+ individuals of each species from multiple sites and 45+ individuals for a selected subset of species. Measurements typically reflect values for individuals though some chemical traits involved composite samples from several individuals at the same site. We also qualitatively characterize each species by plant family, woodiness, functional group, and Raunkiaer lifeform. These data allow us to characterize trait dimensionality, differentiation, and covariation among temperate plant species (e.g., leaf and stem economic syndromes). We can also characterize species’ responses to environmental gradients and drivers of ecological change. With survey and resurvey data available from more than 400 sites in Wisconsin, we can analyze variation in community trait distributions and diversity over time and space. These data thus allow us to assess how trait divergence vs. convergence affect community assembly and how traits may be related to half-century shifts in the distribution and abundance of these species

Induction of Size-Dependent Breakdown of Blood-Milk Barrier in Lactating Mice by TiO₂ Nanoparticles

<div><p>This study aims to investigate the potential nanotoxic effects of TiO₂ nanoparticles (TNPs) to dams and pups during lactation period. TiO₂ nanoparticles are accumulated in mammary glands of lactating mice after i.v. administration. This accumulation of TiO₂ NP likely causes a ROS-induced disruption of tight junction of the blood-milk barrier as indicated by the loss of tight junction proteins and the shedding of alveolar epithelial cells. Compared to larger TNPs (50 nm), smaller ones (8 nm) exhibit a higher accumulation in mammary glands and are more potent in causing perturbations to blood-milk barrier. An alarming finding is that the smaller TNPs (8 nm) are transferred from dams to pups through breastfeeding, likely through the disrupted blood-milk barrier. However, during the lactation period, the nutrient quality of milk from dams and the early developmental landmarks of the pups are not affected by above perturbations.</p></div

Effects of TNPs on mammary gland tight junction proteins ZO-1 and occludin after four doses of TNPs exposure (2, 6, 8 mg/kg) to dams at LDs 2, 4, 6 and 8.

<p>(A) A plausible mechanistic schematic showing TNPs made cell shedding and loose the tight junction between the mammary gland epithelial cells through oxidative stress. (B) Western blot of ZO-1 and occludin in mammary glands. (C) Bar graphs show relative levels of tight junction proteins ZO-1 and occludin by normalizing PBS group to 1.0. The symbol * represents significant difference from the PBS group (P<0.05), (n = 3).</p

Shedding of mammary alveolar epithelial cells induced by TNPs.

<p>A. Schematic anatomical diagrams of lactating mammary glands during lactation period and cartoon indicates that ROS induced cell shedding. B. Representative histological micrographs of the mammary glands 10 days after treatment with (i) PBS; (ii) TNP<b>-</b>8 at a dose of 2 mg/kg; (iii) TNP<b>-</b>8 at a dose of 6 mg/kg; (iv) TNP<b>-</b>8 at a dose of 8 mg/kg. Cell shedding and barrier loosening are noted; (v) Severe cell shedding into alveolar lumen is evident at a dose of 8 mg/kg; (vi) An enlarged view of cell shedding. C. Representative histological micrographs of the mammary glands 10 days after treatment with (i) TNP<b>-</b>50 at a dose of 2 mg/kg; (ii) TNP<b>-</b>50 at a dose of 6 mg/kg; (iii) TNP<b>-</b>50 at a dose of 8 mg/kg; (iv) Cell shedding into alveolar lumen is observed at a dose of 8 mg/kg. D. Quantification of numbers of mammary alveolar epithelial cells shed into the alveolar lumen. There were 7 mice in each experimental group and around 100 alveoli images were examined for each mouse. Scale bar: 40 μm; Narrow arrows indicate gap; Thick arrows indicate cell shedding.</p

Characterization of TNPs.

<p>Characterization of TNPs.</p