Modeling of heavy metals adsorption to a chelating resin in a fluidized bed reactor

Adsorption to a chelating resin (Chelamine Std.) is a method for recovering heavy metals from wastewater contg. very light quantities of heavy metals (<0.3 mol m-3, which approx. corresponds to 20 ppm). A thermodynamical study in a closed vessel showed that equil. is well represented by a Langmuir isotherm. Adsorption kinetics in a continuous stirred tank reactor were also conducted. Expts. were simulated by a global kinetics model comprising mass transfer in a liq. film around the resin particles, with diffusion through the pores and reaction on the adsorption sites. Kinetics has been found to be limited by film mass transfer for all metals studied (Cu2+, Ni2+, Co2+ and Zn2+). The mass transfer coeff. kL was found to be around 10-4 m s-1. Adsorption of heavy metals was then carried out at mini-pilot scale. Problems due to a decrease in particles mean radius during the adsorption prompted us to use a fluidized bed. It is also possible with this reactor to treat solns. contg. suspended solids which would clog fixed beds. The decrease in particle radius (or increase in apparent d. of the resin) produces a contraction of the fluidized bed: unloaded particles remain at the top of the bed and a d. gradient appears throughout the column, leading to a stabilization of the fluidized bed. The measured phenomenon is well described by a liq. plug flow model with immobile resin in the column. As for the adsorption in the continuous stirred tank, the Langmuir model and the kinetics limited by film mass transfer were considered. The mass transfer coeff. kL was adjusted to a value around 10-5 m s-1. [on SciFinder (R)

New Regeneration process of heavy metals loaded chelating resin

An alternative to the classical acid-base regeneration of chelating resins loaded with heavy metals is investigated. The new process consists in recovering the heavy metals with recyclable soluble complexing agents. The semiclosed reactor includes a fixed bed and a stirred tank. A three-parameter model, which implies a double equilibrium in series, is introduced. When less than 10 % of the metal is still fixed on the resin at the end of the desorption, a simplified form of the model with two parameters, which describes a quick equilibrium followed by a first-order kinetics reaction, is proposed. Both forms of the model can simulate results for different experimental conditions (polymer and metal types, polymer initial concentration). It was observed for both cases that the first equilibrium constant depends on the polymer type and that the rate constant of desorption depends on the metal type. The scale-up of desorption is then conducted at mini-pilot scale. Scale-up criteria tend to minimize the desorption time and the soluble polymer quantity used

Scrt1, a transcriptional regulator of β-cell proliferation identified by differential chromatin accessibility during islet maturation.

Glucose-induced insulin secretion, a hallmark of mature β-cells, is achieved after birth and is preceded by a phase of intense proliferation. These events occurring in the neonatal period are decisive for establishing an appropriate functional β-cell mass that provides the required insulin throughout life. However, key regulators of gene expression involved in functional maturation of β-cells remain to be elucidated. Here, we addressed this issue by mapping open chromatin regions in newborn versus adult rat islets using the ATAC-seq assay. We obtained a genome-wide picture of chromatin accessible sites (~ 100,000) among which 20% were differentially accessible during maturation. An enrichment analysis of transcription factor binding sites identified a group of transcription factors that could explain these changes. Among them, Scrt1 was found to act as a transcriptional repressor and to control β-cell proliferation. Interestingly, Scrt1 expression was controlled by the transcriptional repressor RE-1 silencing transcription factor (REST) and was increased in an in vitro reprogramming system of pancreatic exocrine cells to β-like cells. Overall, this study led to the identification of several known and unforeseen key transcriptional events occurring during β-cell maturation. These findings will help defining new strategies to induce the functional maturation of surrogate insulin-producing cells

Source apportionment of methane emissions from the Upper Silesian Coal Basin using isotopic signatures

Anthropogenic emissions are the primary source of the increase in atmospheric methane (CH4) levels. However, estimates of anthropogenic CH4 emissions still show large uncertainties at global and regional scales. Differences in CH4 isotopic source signatures δ13C and δ2H can help to constrain different source contributions (e.g., fossil, waste, agriculture). The Upper Silesian Coal Basin (USCB) represents one of the largest European CH4 emission regions, with more than 500 Gg CH4 yr−1 released from more than 50 coal mine ventilation shafts, landfills, and wastewater treatment plants. During the CoMet (Carbon Dioxide and Methane Mission) campaign in June 2018 methane observations were conducted from a variety of platforms including aircraft and cars to quantify these emissions. Besides the continuous sampling of atmospheric methane concentration, numerous air samples were taken from inside and around the ventilation shafts (1–2 km distance) and aboard the High Altitude and Long Range Research Aircraft (HALO) and DLR Cessna Caravan aircraft, and they were analyzed in the laboratory for the isotopic composition of CH4. The airborne samples downwind of the USCB contained methane from the entire region and thus enabled determining the mean signature of the USCB accurately. This mean isotopic signature of methane emissions was -50.9±0.7 ‰ for δ13C and -226±9 ‰ for δ2H. This is in the range of previous USCB studies based on samples taken within the mines for δ13C but more depleted in δ2H than reported before. Signatures of methane enhancements sampled upwind of the mines and in the free troposphere clearly showed the influence of biogenic sources. We determined the source signatures of individual coal mine ventilation shafts using ground-based samples. These signatures displayed a considerable range between different mines and also varied for individual shafts from day to day. Different layers of the USCB coal contain thermogenic methane, isotopically similar to natural gas, and methane formed through biogenic carbonate reduction. The signatures vary depending on what layer of coal is mined at the time of sampling. Mean shaft signatures range from −60 ‰ to −42 ‰ for δ13C and from −200 ‰ to −160 ‰ for δ2H. A gradient in the signatures of subregions of the USCB is reflected both in the aircraft data and in the ground samples, with emissions from the southwest being most depleted in δ2H and emissions from the south being most depleted in δ13C, which is probably associated with the structural and lithostratigraphic history of the USCB and generation and migration processes of methane in the coal. The average signature of -49.8±5.7 ‰ in δ13C and -184±32 ‰ in δ2H from the ventilation shafts clearly differs from the USCB regional signature in δ2H. This makes a source attribution using δ2H signatures possible, which would not be possible with only the δ13C isotopic signatures. We assume that the USCB plume mainly contains fossil coal mine methane and biogenic methane from waste treatment, because the USCB is a highly industrialized region with few other possible methane sources. Assuming a biogenic methane signature between and −320 ‰ and −280 ‰ for δ2H, the biogenic methane emissions from the USCB account for 15 %–50 % of total emissions. The uncertainty range shows the need of comprehensive and extensive sampling from all possible source sectors for source apportionment. The share of anthropogenic–biogenic emissions of 0.4 %–14 % from this densely populated industrial region is underestimated in commonly used emission inventories. Generally, this study demonstrates the importance of δ2H-CH4 observations for methane source apportionment in regions with a mix of thermogenic and biogenic sources and, especially in our case, where the δ13C signature of the coal mine gas has a large variability.</p

Lymphocyte-Derived Exosomal MicroRNAs Promote Pancreatic β Cell Death and May Contribute to Type 1 Diabetes Development.

Type 1 diabetes is an autoimmune disease initiated by the invasion of pancreatic islets by immune cells that selectively kill the β cells. We found that rodent and human T lymphocytes release exosomes containing the microRNAs (miRNAs) miR-142-3p, miR-142-5p, and miR-155, which can be transferred in active form to β cells favoring apoptosis. Inactivation of these miRNAs in recipient β cells prevents exosome-mediated apoptosis and protects non-obese diabetic (NOD) mice from diabetes development. Islets from protected NOD mice display higher insulin levels, lower insulitis scores, and reduced inflammation. Looking at the mechanisms underlying exosome action, we found that T lymphocyte exosomes trigger apoptosis and the expression of genes involved in chemokine signaling, including Ccl2, Ccl7, and Cxcl10, exclusively in β cells. The induction of these genes may promote the recruitment of immune cells and exacerbate β cell death during the autoimmune attack. Our data point to exosomal-miRNA transfer as a communication mode between immune and insulin-secreting cells

Epidermolysa bullosa in Danish Hereford calves is caused by a deletion in LAMC2 gene

BACKGROUND Heritable forms of epidermolysis bullosa (EB) constitute a heterogeneous group of skin disorders of genetic aetiology that are characterised by skin and mucous membrane blistering and ulceration in response to even minor trauma. Here we report the occurrence of EB in three Danish Hereford cattle from one herd. RESULTS Two of the animals were necropsied and showed oral mucosal blistering, skin ulcerations and partly loss of horn on the claws. Lesions were histologically characterized by subepidermal blisters and ulcers. Analysis of the family tree indicated that inbreeding and the transmission of a single recessive mutation from a common ancestor could be causative. We performed whole genome sequencing of one affected calf and searched all coding DNA variants. Thereby, we detected a homozygous 2.4 kb deletion encompassing the first exon of the LAMC2 gene, encoding for laminin gamma 2 protein. This loss of function mutation completely removes the start codon of this gene and is therefore predicted to be completely disruptive. The deletion co-segregates with the EB phenotype in the family and absent in normal cattle of various breeds. Verifying the homozygous private variants present in candidate genes allowed us to quickly identify the causative mutation and contribute to the final diagnosis of junctional EB in Hereford cattle. CONCLUSIONS Our investigation confirms the known role of laminin gamma 2 in EB aetiology and shows the importance of whole genome sequencing in the analysis of rare diseases in livestock

A circular RNA generated from an intron of the insulin gene controls insulin secretion.

Fine-tuning of insulin release from pancreatic β-cells is essential to maintain blood glucose homeostasis. Here, we report that insulin secretion is regulated by a circular RNA containing the lariat sequence of the second intron of the insulin gene. Silencing of this intronic circular RNA in pancreatic islets leads to a decrease in the expression of key components of the secretory machinery of β-cells, resulting in impaired glucose- or KCl-induced insulin release and calcium signaling. The effect of the circular RNA is exerted at the transcriptional level and involves an interaction with the RNA-binding protein TAR DNA-binding protein 43 kDa (TDP-43). The level of this circularized intron is reduced in the islets of rodent diabetes models and of type 2 diabetic patients, possibly explaining their impaired secretory capacity. The study of this and other circular RNAs helps understanding β-cell dysfunction under diabetes conditions, and the etiology of this common metabolic disorder

A circular RNA generated from an intron of the insulin gene controls insulin secretion

Fine-tuning of insulin release from pancreatic β-cells is essential to maintain blood glucose homeostasis. Here, we report that insulin secretion is regulated by a circular RNA containing the lariat sequence of the second intron of the insulin gene. Silencing of this intronic circular RNA in pancreatic islets leads to a decrease in the expression of key components of the secretory machinery of β-cells, resulting in impaired glucose- or KCl-induced insulin release and calcium signaling. The effect of the circular RNA is exerted at the transcriptional level and involves an interaction with the RNA-binding protein TAR DNA-binding protein 43 kDa&nbsp;(TDP-43). The level of this circularized intron is reduced in the islets of rodent diabetes models and of type 2 diabetic patients, possibly explaining their impaired secretory capacity. The study of this and other circular RNAs helps understanding β-cell dysfunction under diabetes conditions, and the etiology of this common metabolic disorder

A COL7A1 Mutation Causes Dystrophic Epidermolysis Bullosa in Rotes Höhenvieh Cattle

We identified a congenital mechanobullous skin disorder in six calves on a single farm of an endangered German cattle breed in 2010. The condition presented as a large loss of skin distal to the fetlocks and at the mucosa of the muzzle. All affected calves were euthanized on humane grounds due to the severity, extent and progression of the skin and oral lesions. Examination of skin samples under light microscopy revealed detachment of the epidermis from the dermis at the level of the dermo epidermal junction, leading to the diagnosis of a subepidermal bullous dermatosis such as epidermolysis bullosa. The pedigree was consistent with monogenic autosomal recessive inheritance. We localized the causative mutation to an 18 Mb interval on chromosome 22 by homozygosity mapping. The COL7A1 gene encoding collagen type VII alpha 1 is located within this interval and COL7A1 mutations have been shown to cause inherited dystrophic epidermolysis bullosa (DEB) in humans. A SNP in the bovine COL7A1 exon 49 (c.4756C>T) was perfectly associated with the observed disease. The homozygous mutant T/T genotype was exclusively present in affected calves and their parents were heterozygous C/T confirming the assumed recessive mode of inheritance. All known cases and genotyped carriers were related to a single cow, which is supposed to be the founder animal. The mutant T allele was absent in 63 animals from 24 cattle breeds. The identified mutation causes a premature stop codon which leads to a truncated protein representing a complete loss of COL7A1 function (p.R1586*). We thus have identified a candidate causative mutation for this genetic disease using only three cases to unravel its molecular basis. Selection against this mutation can now be used to eliminate the mutant allele from the Rotes Höhenvieh breed