Mercury abatement in the environment: Insights from industrial emissions and fates in the environment.

Mercury's neurotoxic effects have prompted the development of advanced control and remediation methods to meet stringent measures for industries with high-mercury feedstocks. Industries with significant Hg emissions, including artisanal and small-scale gold mining (ASGM)-789.2 Mg year-1, coal combustion-564.1 Mg year-1, waste combustion-316.1 Mg year-1, cement production-224.5 Mg year-1, and non-ferrous metals smelting-204.1 Mg year-1, use oxidants and adsorbents capture Hg from waste streams. Oxidizing agents such as O3, Cl2, HCl, CaBr2, CaCl2, and NH4Cl oxidize Hg0 to Hg2+ for easier adsorption. To functionalize adsorbents, carbonaceous ones use S, SO2, and Na2S, metal-based adsorbents use dimercaprol, and polymer-based adsorbents are grafted with acrylonitrile and hydroxylamine hydrochloride. Adsorption capacities span 0.2-85.6 mg g-1 for carbonaceous, 0.5-14.8 mg g-1 for metal-based, and 168.1-1216 mg g-1 for polymer-based adsorbents. Assessing Hg contamination in soils and sediments uses bioindicators and stable isotopes. Remediation approaches include heat treatment, chemical stabilization and immobilization, and phytoremediation techniques when contamination exceeds thresholds. Achieving a substantially Hg-free ecosystem remains a formidable challenge, chiefly due to the ASGM industry, policy gaps, and Hg persistence. Nevertheless, improvements in adsorbent technologies hold potential.

Assessment of the emission factors for potentially toxic elements from coal-fired boilers and sintering furnaces in a steel production plant.

The emission factor (EF), the weight of potentially toxic elements (PTEs) per unit energy or weight of sinter produced were evaluated for coal-fired boilers and sintering furnaces integrated in a steel plant. From three coal-fired boilers, 15 samples were taken while 22 samples were taken from four sintering furnaces. Investigations were performed on the EF of lead, cadmium, mercury, arsenic and chromium (VI). The coefficient of variance for the first 3 samples from each PTE was used to decide whether 2 more samples were necessary for the investigation. Three samples were sufficient for Cr (VI), however, 5 samples were required for Pb, Cd, Hg, and As, since the variances in concentrations of the first three samples exceeded 20%. The ranges for the ratio of the laboratory-based EF to the default EF applied by the Environment Protection Administration (EPA Taiwan) for Pb, Cd, Hg, and As for the coal-fired boiler were 0.08-0.013, 0.014-0.017, 0.019-0.033, 0.047-0.066 and for the sintering furnaces were 0.059-0.232, 0.05-0.151, 0.05-0.364, and 0.067-0.824. The ratio for Cr (VI)- was constant at 0.005 for all the coal fired boilers while it ranged from 0.057-0.709 for the sintering furnaces. Whilst source identification, enrichment factors, and spatial distributions for PTEs are often studied, laboratory-based investigations on the EFs for PTEs from industrial plants are rarely performed. This study filled the information gap and compared the obtained EFs with the EPA default values. To avoid overcharging industrial plants equipped with the best available technology for emission control, the EPA should apply field investigations and laboratory-based EFs instead of the default EPA EFs to calculate air pollution fees. Insights from this investigation can be applied to promote the adoption of appropriate air pollution control devices to cut down the emission of PTEs.

MicroRNA-29a represses osteoclast formation and protects against osteoporosis by regulating PCAF-mediated RANKL and CXCL12.

Osteoporosis deteriorates bone mass and biomechanical strength, becoming a life-threatening cause to the elderly. MicroRNA is known to regulate tissue remodeling; however, its role in the development of osteoporosis remains elusive. In this study, we uncovered that silencing miR-29a expression decreased mineralized matrix production in osteogenic cells, whereas osteoclast differentiation and pit formation were upregulated in bone marrow macrophages as co-incubated with the osteogenic cells in transwell plates. In vivo, decreased miR-29a expression occurred in ovariectomy-mediated osteoporotic skeletons. Mice overexpressing miR-29a in osteoblasts driven by osteocalcin promoter (miR-29aTg/OCN) displayed higher bone mineral density, trabecular volume and mineral acquisition than wild-type mice. The estrogen deficiency-induced loss of bone mass, trabecular morphometry, mechanical properties, mineral accretion and osteogenesis of bone marrow mesenchymal cells were compromised in miR-29aTg/OCN mice. miR-29a overexpression also attenuated the estrogen loss-mediated excessive osteoclast surface histopathology, osteoclast formation of bone marrow macrophages, receptor activator nuclear factor-κ ligand (RANKL) and C-X-C motif chemokine ligand 12 (CXCL12) expression. Treatment with miR-29a precursor improved the ovariectomy-mediated skeletal deterioration and biomechanical property loss. Mechanistically, miR-29a inhibited RANKL secretion in osteoblasts through binding to 3'-UTR of RANKL. It also suppressed the histone acetyltransferase PCAF-mediated acetylation of lysine 27 in histone 3 (H3K27ac) and decreased the H3K27ac enrichment in CXCL12 promoters. Taken together, miR-29a signaling in osteogenic cells protects bone tissue from osteoporosis through repressing osteoclast regulators RANKL and CXCL12 to reduce osteoclastogenic differentiation. Arrays of analyses shed new light on the miR-29a regulation of crosstalk between osteogenic and osteoclastogenic cells. We also highlight that increasing miR-29a function in osteoblasts is beneficial for bone anabolism to fend off estrogen deficiency-induced excessive osteoclastic resorption and osteoporosis.

Dynamic analysis of the human brain with complex cerebral sulci.

The brain is one of the most vulnerable organs inside the human body. Head accidents often appear in daily life and are easy to cause different level of brain damage inside the skull. Once the brain suffered intense locomotive impact, external injuries, falls, or other accidents, it will result in different degrees of concussion. This study employs finite element analysis to compare the dynamic characteristics between the geometric models of an assumed simple brain tissue and a brain tissue with complex cerebral sulci. It is aimed to understand the free vibration of the internal brain tissue and then to protect the brain from injury caused by external influences. Reverse engineering method is used for a Classic 5-Part Brain (C18) model produced by 3B Scientific Corporation. 3D optical scanner is employed to scan the human brain structure model with complex cerebral sulci and imported into 3D graphics software to construct a solid brain model to simulate the real complex brain tissue. Obtaining the normal mode analysis by inputting the material properties of the true human brain into finite element analysis software, and then to compare the simplified and the complex of brain models.