Mature fine tailings (MFT) are a by-product of oil sands mining that must be reclaimed through capping or use as a reclamation substrate. Some chemical and physical properties of MFT make it inhospitable for plant growth, such as high concentrations of sodium, sulfate, chloride, and hydrocarbons. A greenhouse study assessed whether substrates of various mixes of dry MFT, overburden sand, and peat mineral soil mix (PMM) and caps of forest floor organic material (LFH) and PMM would support the emergence and growth of three native grass species commonly used in land reclamation. Select vegetation properties were monitored for 16 wk in the greenhouse; select chemical and physical substrate properties were determined in the laboratory. was more tolerant of dry MFT than and . Mean aboveground and belowground biomass were more than twice as high on substrates with <60% MFT than on 100% MFT. Aboveground biomass was two to four times greater with capping than without and 30% greater on LFH than PMM caps. Cover and density followed similar trends. Belowground biomass on capped substrates was at least double that on uncapped substrates. Aboveground biomass was almost doubled with the use of fertilizer. High concentrations of hydrocarbons and exchangeable ions were associated with reduced plant growth and health. Results from this study show that capping, amendments, and fertilizer may improve the reclamation potential of dry MFT.
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http://dx.doi.org/10.2134/jeq2013.10.0415 | DOI Listing |
Front Neurol
December 2024
Department of Physiology, University of Kentucky, Lexington, KY, United States.
Auditory hair cells form precise and sensitive staircase-like actin protrusions known as stereocilia. These specialized microvilli detect deflections induced by sound through the activation of mechano-electrical transduction (MET) channels located at their tips. At rest, a small MET channel current results in a constant calcium influx which regulates the morphology of the actin cytoskeleton in the shorter 'transducing' stereocilia.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Oral Biology, Rutgers School of Dental Medicine, Newark, NJ 07103, USA.
Patients with diabetes mellitus (DM) have an increased risk of tooth decay caused by alterations in their tooth development and their oral environment, as well as a tendency to present with pulp infection due to compromised immune response. The present study analyzed the characteristic alterations in tooth development under DM conditions using incisors from type 2 diabetic mouse model (T2DM mice). In micro-CT analyses, T2DM mice showed delayed dentin and enamel formation.
View Article and Find Full Text PDFWorld J Clin Cases
January 2025
Department of Obstetrics and Gynecology, Saku Central Hospital Advanced Care Center, Saku City 385-0051, Nagano, Japan.
Background: Malignant transformation (MT) of mature cystic teratoma (MCT) has a poor prognosis, especially in advanced cases. Concurrent chemoradiotherapy (CCRT) has an inhibitory effect on MT.
Case Summary: Herein, we present a case in which CCRT had a reduction effect preoperatively.
bioRxiv
December 2024
Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
To myelinate axons, oligodendrocyte precursor cells (OPCs) must stop dividing and differentiate into premyelinating oligodendrocytes (preOLs). PreOLs are thought to survey and begin ensheathing nearby axons, and their maturation is often stalled at human demyelinating lesions. Lack of genetic tools to visualize and manipulate preOLs has left this critical differentiation stage woefully understudied.
View Article and Find Full Text PDFEMBO J
January 2025
Telethon Institute of Genetics and Medicine (TIGEM), 80078, Pozzuoli, Italy.
Endoplasmic reticulum (ER) plasticity and ER-phagy are intertwined processes essential for maintaining ER dynamics. We investigated the interplay between two isoforms of the ER-phagy receptor FAM134B in regulating ER remodeling in differentiating myoblasts. During myogenesis, the canonical FAM134B1 is degraded, while its isoform FAM134B2 is transcriptionally upregulated.
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