High frequency Lunar Penetrating Radar quality control, editing and processing of Chang'E-4 lunar mission.

Chinese lunar landing mission Chang'E-4 reached the far side of the Moon in January 2019 and has been providing unprecedented Lunar Penetrating Radar data able to explore the lunar subsurface down to more than 40 m (with its more resolutive high frequency band). Data are periodically released to the scientific community in raw PDS4 format. Here we provide different versions of the radar dataset after editing (i.e. pre-processing), partial, and full processing in order to provide a complete ready-to-use dataset to end-users (data collected since 4th January 2019 until 27th March 2023) which can be directly exploited for analysis, interpretation, inversion, as well as integration with imagery or other information. In particular, we implemented an efficient and objective way to remove duplicated traces representing more than 90% of original data, as well as a processing flow able to retain all the original data information, while avoiding redundancies. The provided datasets can be implemented with future data releases and straightforwardly exploited for any future analysis.

New approach for regulation of the internal recirculation flow rate by fuzzy logic in biological wastewater treatments.

The internal recirculation plays an important role on the different biological processes of wastewater treatment plants because it has a great influence on the concentration of pollutants, especially nutrients. Usually, the internal recirculation flow rate is kept fixed or manipulated by control techniques to maintain a fixed nitrate set-point in the last anoxic tank. This work proposes a new control strategy to manipulate the internal recirculation flow rate by applying a fuzzy controller. The proposed controller takes into account the effects of the internal recirculation flow rate on the inlet of the biological treatment and on the denitrification and nitrification processes with the aim of reducing violations of legally established limits of nitrogen and ammonia and also reducing operational costs. The proposed fuzzy controller is tested by simulation with the internationally known benchmark simulation model no. 2. The objective is to apply the proposed fuzzy controller in any control strategy, only replacing the manipulation of the internal recirculation flow rate, to improve the plant operation.Therefore, it has been implemented in five operation strategies from the literature, replacing their original internal recirculation flow rate control, and simulation results are compared with those of the original strategies. Results show improvements with the application of the proposed fuzzy controller of between 2.25 and 57.94% in reduction of total nitrogen limit violations, between 55.22 and 79.69% in reduction of ammonia limit violations and between 0.84 and 38.06% in cost reduction of pumping energy.

Carcass and meat quality of young Angus steers with different growth potential finished exclusively grass-fed or corn supplemented.

Beef cattle production has a large variety of systems with different performance and technology levels. This study compared young Angus steers carcass and meat quality traits of high growth potential early-finished animals fed exclusively on pasture with low growth potential late-finished animals. Besides the grazed forage, the low growth potential group received corn grain at 0.8% of their body weight right after the slaughtering of the first group. Following weaning, the 20 steers grazed pastures composed of oat, ryegrass, and clovers. At winter's onset, animals were moved to native pastures improved with fescue and clovers. The supplemented period of late steers began when the first group of ten early-finished animals reached the requirements for slaughter. Supplementation ended when the animals got the slaughter requirements. The high growth potential steers showed a ribeye area (P < 0.0001) and a Longissimus muscle width highly significantly (P < 0.0001) superior to the low growth group. However, corn-supplemented animals showed better dressing percentage (P < 0.0001), subcutaneous fat thickness (P < 0.0001), marbling (P < 0.0001), and muscle (P = 0.0033) scores, but lower shear force (P = 0.0001). The finishing system did impact fat lightness (L*; P = 0.0234) at the slaughter time. Grass-fed animals showed higher red-green color parameter (a*) values than corn supplemented on fat at 24 h (P = 0.0439) but lower hue angle (P = 0.0418). The consumer panel showed better results for tenderness and general acceptability for supplemented animals beef compared to grass-fed. The supplementation resulted in a higher carcass standardization. It also provided higher PUFA: MUFA and n-6: n-3 ratios, and a higher amount of n-3. Supplemental corn grain did not have adverse effects upon the beneficial effects to human health of the grass-fed beef.

Fuzzy logic for plant-wide control of biological wastewater treatment process including greenhouse gas emissions.

The application of control strategies is increasingly used in wastewater treatment plants with the aim of improving effluent quality and reducing operating costs. Due to concerns about the progressive growth of greenhouse gas emissions (GHG), these are also currently being evaluated in wastewater treatment plants. The present article proposes a fuzzy controller for plant-wide control of the biological wastewater treatment process. Its design is based on 14 inputs and 6 outputs in order to reduce GHG emissions, nutrient concentration in the effluent and operational costs. The article explains and shows the effect of each one of the inputs and outputs of the fuzzy controller, as well as the relationship between them. Benchmark Simulation Model no 2 Gas is used for testing the proposed control strategy. The results of simulation results show that the fuzzy controller is able to reduce GHG emissions while improving, at the same time, the common criteria of effluent quality and operational costs.

Control strategies for nitrous oxide emissions reduction on wastewater treatment plants operation.

The present paper focused on reducing greenhouse gases emissions in wastewater treatment plants operation by application of suitable control strategies. Specifically, the objective is to reduce nitrous oxide emissions during the nitrification process. Incomplete nitrification in the aerobic tanks can lead to an accumulation of nitrite that triggers the nitrous oxide emissions. In order to avoid the peaks of nitrous oxide emissions, this paper proposes a cascade control configuration by manipulating the dissolved oxygen set-points in the aerobic tanks. This control strategy is combined with ammonia cascade control already applied in the literature. This is performed with the objective to take also into account effluent pollutants and operational costs. In addition, other greenhouse gases emissions sources are also evaluated. Results have been obtained by simulation, using a modified version of Benchmark Simulation Model no. 2, which takes into account greenhouse gases emissions. This is called Benchmark Simulation Model no. 2 Gas. The results show that the proposed control strategies are able to reduce by 29.86% of nitrous oxide emissions compared to the default control strategy, while maintaining a satisfactory trade-off between water quality and costs.

Candidate genes for type 1 diabetes modulate pancreatic islet inflammation and ß-cell apoptosis.

Genome-wide association studies (GWAS) have identified more than 50 loci associated with genetic risk of type 1 diabetes (T1D). Several T1D candidate genes have been suggested or identified within these regions, but the molecular mechanisms by which they contribute to insulitis and ß-cell destruction remain to be clarified. More than 60% of the T1D candidate genes are expressed in human pancreatic islets, suggesting that they contribute to T1D by regulating at least in part pathogenic mechanisms at the ß-cell level. Recent studies by our group indicate that important genetically regulated pathways in ß-cells include innate immunity and antiviral activity, involving RIG-like receptors (particularly MDA5) and regulators of type I IFNs (i.e. PTPN2 and USP18), and genes related to ß-cell phenotype and susceptibility to pro-apoptotic stimuli (i.e. GLIS3). These observations reinforce the concept that the early pathogenesis of T1D is characterized by a dialogue between the immune system and pancreatic ß-cells. This dialogue is probably influenced by polymorphisms in genes expressed at the ß-cell and/or immune system level, leading to inadequate responses to environmental cues such as viral infections. Further studies are needed to clarify how these disease-associated variants affect pancreatic ß-cell responses to inflammation and the subsequent triggering of autoimmune responses and progressive ß-cell loss.

USP18 is a key regulator of the interferon-driven gene network modulating pancreatic beta cell inflammation and apoptosis.

Type 1 diabetes (T1D) is an autoimmune disease targeting pancreatic beta cells. Genome-wide association studies and gene expression analysis identified interferon (IFN)-driven gene networks as crucial pathways in the pathogenesis of T1D. IFNs are linked to the response to viral infections and might contribute to the initiation of the autoimmune process in T1D. We presently analyzed the role of ubiquitin-specific peptidase 18 (USP18), an interferon-stimulated gene 15-specific protease, on IFN-induced pancreatic beta cell inflammation and apoptosis. Our findings indicate that USP18 inhibition induces inflammation by increasing the STAT signaling and exacerbates IFN-induced beta cell apoptosis by the mitochondrial pathway of cell death. USP18 regulates activation of three BH3-only proteins, namely, DP5, Bim and PUMA in pancreatic beta cells, suggesting a direct link between regulators of the type I IFN signaling pathway and members of the BCL-2 family. USP18 depletion increases the expression of the T1D candidate gene MDA5, leading to an upregulation of double-stranded RNA-induced chemokine production. These data suggest a cross talk between the type I IFN signaling pathway and a candidate gene for T1D to increase pro-inflammatory responses in beta cells. The present study shows that USP18 is a key regulator of IFN signaling in beta cells and underlines the importance of this pathway in beta cell inflammation and death.

Exploring the diabetogenicity of the HLA-B18-DR3 CEH: independent association with T1D genetic risk close to HLA-DOA.

The objective of this study was to identify additional diabetes susceptibility markers in the MHC that could be responsible for the differential diabetogenicity of different HLA-DR3 CEHs. High-resolution SNP genotyping of the MHC was carried out in 15 type 1 diabetes (T1D) patients and 39 non-diabetic controls, homozygous for DR3-DQ2 and with one copy of the A(*)30-B(*)18-MICA(*)4-F1C30-DRB1(*)0301-DQB1(*)0201-DPB1(*)0202 HLA haplotype. Significantly associated SNPs were replicated in an independent sample of 554 T1D patients and 841 controls without HLA matching. Electrophoretic mobility shift assay was used to show a functional effect of an associated SNP. Seven SNPs showed evidence of association in the initial discovery experiment. Upon replication, only rs419434 (upstream HLA-DOA gene) remained significant. A functional variant (rs432375) in complete LD with rs419434 was shown to affect USF-1 binding and could be responsible for the association signal in the region. We have identified a new susceptibility locus within the MHC with a modest contribution to T1D (OR=1.93; CI: 1.52-2.44; P=10(-8)) that is independent of HLA-DRB1 locus.

The functional R620W variant of the PTPN22 gene is associated with celiac disease.

The functional (R620W) variant of human PTPN22 (protein tyrosine phosphatase non-receptor 22) gene has been implicated in the risk to several autoimmune disorders, including type 1 diabetes, Graves' disease, rheumatoid arthritis and systemic lupus erythematosus. In an association study of this single nucleotide polymorphism with celiac disease (CD), comparison of 262 young diagnosis patients and 214 adult controls from Spain showed a higher frequency of the minor allele in the CD group (9.7% vs 5.6% in controls; P = 0.018), suggestive of an increased genetic risk to the disease (odds ratio = 1.82; 95% confidence interval 1.1-3.0). These results support the role of PTPN22 as a general autoimmunity locus involved in tolerance induction in the thymus.

Toll-like receptor 4 (TLR4) gene polymorphisms in celiac disease.

Toll-like receptors (TLRs) participate in the first line of immune defense through antigen pattern recognition, and ligands include exogenous and host-derived molecules. Coding variants in TLR4 have been associated with autoimmune diseases like ulcerative colitis, Crohn's disease, and rheumatoid arthritis. Our aim was to determine whether these polymorphisms are associated with celiac disease (CD). Two coding single nucleotide polymorphisms of TLR4 (Asp299Gly and Thr399Ile) were genotyped in 95 family trios with CD as well as in 186 patients and 186 unrelated controls. There were no differences in allele, genotype or haplotype distribution, or transmission between patient and control groups. Our results do not support association of these TLR4 variants with CD.

Association of KIR2DL5B gene with celiac disease supports the susceptibility locus on 19q13.4.

Genome-wide scans have detected linkage to celiac disease (CD) in several genomic locations, including 19q13.4. Killer immunoglobulin-like receptor (KIR) genes map to the region and encode receptors of natural killer (NK) cells and certain T cells that modulate cytolitic activity through interactions with HLA class I ligands, participating in the innate immune response. We performed KIR genotyping in a group of 70 CD patients of Basque origin and compared gene content, genotype and haplotype frequencies to ethnically matched blood-donors. The frequency of gene combination KIR2DL5B(+)/KIR2DL5A(-) was significantly higher in the disease group, and this result was confirmed in a second group of 343 CD patients and 160 controls of Spanish origin, suggesting an implication of this 'unexpressed' gene with increased susceptibility to CD (combined OR of 3.63 (95% CI: 1.76-7.51; P=0.0004)), possibly due to the lack of an efficient inhibitory signal. Our results support the role of the KIR gene cluster in celiac disease and replicate the CD-susceptibility locus at 19q13.4.