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The effects of three oxidation processes, ozone (O3) oxidation, O3/potassium peroxymonosulfate (PMS) oxidation, and O3/hydrogen peroxide (H2O2) oxidation, on the treatment of phosphating wastewater were compared. Additionally, the quality of effluent was analyzed through measurements of COD, UV254, and three-dimensional fluorescence spectra, highlighting the influence of various advanced oxidation processes on the wastewater effluent quality and the removal pathways. The results showed that increasing the ozone dosage and adding appropriate amounts of PMS and H2O2 could enhance the removal of organic contaminants from phosphating wastewater. With initial COD of (130±20) mg/L, reaction time of 120 minutes, and ozone dosage of 7.65 mg/min, the COD removal rate was only 37% by the ozonation process, the COD removal rate reached 45.65% by the O3/PMS oxidation process with PMS mass concentration of 2 g/L, the COD removal rate reached 58.3% by the O3/H2O2 oxidation process with 0.5 g/L dosage of H2O2 (30% concentration). Among the three methods, the O3/H2O2 process demonstrated the highest efficacy in removing COD from phosphating wastewater, as the synergistic production of more highly oxidative free radicals by O3 and H2O2 enhancd the oxidation capacity of the system. All three processes effectively degraded aromatic compounds and fluorescent substances in wastewater, while the individual O3 oxidation and the O3/PMS process mainly degraded substances resembling proteins into fulvic and humic-like materials, and the O3/H2O2 oxidation process could further degrade these fulvic and humic-like substances.

Diatoms (> 2 μm) have traditionally been identified as the primary biological agents linking the carbon (C) and silicon (Si) cycles. However, recent research has shown that picophytoplankton species (< 2 μm) also play a crucial role in the intertwined Si-C biogeochemical cycling in marine ecosystems. In this study, we examined the spatial distribution and vertical variation of micro/nano-diatoms and picophytoplankton in the eastern Indian Ocean (EIO), aimed to differentiate the contributions of living carbon and biogenic silica (bSi) stocks between diatoms and picophytoplankton. The study revealed that the abundance of picophytoplankton surpasses that of diatoms by four to seven orders of magnitude. Synechococcus was predominantly presented in the upper layer, while Prochlorococcus, picoeukaryotes, and diatoms were primarily located in the middle layer. Aggregation Boosted Tree (ABT) and Generalized Additive Models (GAM) analyses revealed that temperature and silicate (DSi) levels strongly influenced the diatom and picophytoplankton communities in the EIO. The fractions smaller than 2 μm made substantial contributions of 86.20%, 55.69%, and 96.86% to chlorophyll a (Chl-a), particulate organic carbon (POC), and living carbon biomass, respectively, underscoring the ecological significance of picophytoplankton in the carbon cycle of oligotrophic regions. Picophytoplankton represented a 33.06% of bSi stocks in the area, comparable to the contribution of diatoms (> 20 μm). Moreover, estimated contributions of diatom living carbon and silicon quota averaged 0.47% and 0.66%, respectively, while that of Synechococcus stood at 2.58% and 1.77%, indicating the predominance of Synechococcus as a weakly siliceous organism with high cell abundance in oligotrophic seas. Overall, this study draws on data from diatom and picophytoplankton biomass in the EIO to offer insights into the disproportionate carbon and silicon budgets in oligotrophic oceans from a biological perspective.

The color of light affects the reproductive performance of poultry, but it is not clear what efficient illumination strategy could be adopted to improve the reproductive performance of Zi-goose. Red light can increase the average weekly egg production rate, egg production, and qualified production. It can increase the serum GnRH level and decrease the serum PRL, MT, and T4 levels. In our study, red light for 12 h increased the average weekly laying rate, average qualified egg production, and hatching rate of Zi-goose eggs, and increased the serum levels of FSH, LH, P4, E2, MT, T3, and T4. Blue light at 14 h improved the average weekly egg production rate, average egg production, and average qualified egg production, and reduce serum PRL and MT levels to ensure the improvement of reproductive performance of goose. A total of 705,714 overlapping group sequences, 471,145 transcript sequences, and 268,609 single gene sequences were obtained from 18 sequencing samples, with a total length of 323.04, 668.53, and 247.88 M, respectively. About 176,416 unigenes were annotated successfully in six databases, accounting for 65.68% of the total unigenes obtained. 2,106, 2,142, and 8,892 unigenes were identified in the hypothalamus, pituitary gland, and ovary of the birds respectively, with different expressions of light regulation. The hypothalamus, ovary, and pituitary were involved in 279, 327, and 275 KEGG (Kyoto Encyclopedia of Genes and Genomes) metabolic pathways in response to light, respectively. Through further significance analysis and differential discovery rate control, a total of five metabolic pathways were obtained which were closely related to the reproductive hormones of goose. Ten candidate genes related to the reproductive performance of goslings were selected according to the identification results of differentially expressed genes of goslings under red light and white light conditions and the genes involved in metabolic pathways significantly related to the reproductive hormones of goslings. The expression levels of GnRh-1 in the hypothalamus, GnRH-R, FSHβ and LHβ in the pituitary gland, and FSH-R and LH-R candidate genes in the ovary were higher under the 12 h red light treatment than white light. However, the expression levels of VIP, PRL, and PRL-R candidate genes in the hypothalamus, pituitary and ovary were lower under 12 h red light than under 12 h white light.

Abstract Escherichia coli has become one of the most important causes of calf diarrhea. The aim of this study is to determine the patterns of antimicrobial resistance of E. coli isolates from six cattle farms and to identify prominent resistance genes and virulence genes among the strains isolated from the diarrhea of calves. Antimicrobial susceptibility tests were performed using the disk diffusion method, and PCR was used to detect resistance and virulence genes. The prevalence of multidrug resistant (MDR) E. coli was 77.8% in dairy cattle and 63.6% in beef cattle. There were high resistance rates to penicillin (100%, 100%) and ampicillin (96.3%, 86.4%) in E. coli from dairy cattle and beef cattle. Interestingly, resistance rate to antimicrobials and distribution of resistance genes in E. coli isolated from dairy cattle were higher than those in beef cattle. Further analysis showed that the most prevalent resistance genes were bla TEM and aadA1 in dairy cattle and beef cattle, respectively. Moreover, seven diarrheagenic virulence genes (irp2, fyuA, Stx1, eaeA, F41, K99 and STa) were present in the isolates from dairy cattle, with a prevalence ranging from 3.7% to 22.22%. Six diarrheagenic virulence genes (irp2, fyuA, Stx1, eaeA, hylA and F41) were identified in the isolates from beef cattle, with a prevalence ranging from 2.27% to 63.64%. Our results provide important evidence for better exploring their interaction mechanism. Further studies are also needed to understand the origin and transmission route of E. coli in cattle to reduce its prevalence.

In this study, we investigated the protective effect of Astragaloside IV (Ast) on mouse podocytes and its possible mechanism of action by constructing a cadmium-induced mouse renal podocytes model. We investigated the effects of cadmium (Cd) toxicity on cell number, morphology, the mitochondrial status of subcellular organelles, protein and gene levels, and the protective effects of Ast by constructing a model of Cd-induced damage to mouse renal podocytes (MPC5) and giving Ast protection at the same time. The results showed that exposure of MPC5 cells to CdCl2 culture medium containing 6.25 μM concentration acted with low cell mortality, but the mortality of MPC5 cells increased with the prolongation of cadmium exposure time. Given Ast, the death rate in the low dose group (12.5 μM) was significantly reduced, while the death rate in the medium dose group (25 μM) was extremely significantly reduced. In comparison to the control group, the Cd-exposed group exhibited a significant increase of 166.7% in malondialdehyde (MDA) content and a significant decrease of 17.1% in SOD activity. The mitochondrial membrane potential was also reduced to varying degrees. However, in the Ast-protected group compared to the Cd-exposed group, the MDA content significantly decreased by 20.8%, the SOD activity decreased by 7.14%, and the mitochondrial membrane potential showed a significant increase. Fluorescence staining of mitochondrial membrane potential indicated that Cd exposure caused mitochondrial apoptosis. In the 12-h cadmium-exposed group, the protein expression of Nephrin in mice significantly decreased by 33.4%. However, the expression of the Desmin protein significantly increased by 67.8%, and the expression of the autophagy protein LC3-II significantly increased by 55.5%. Meanwhile, the expression of PINK1, a mitochondrial autophagy pathway protein, was significantly increased in the 12 h and 24 h cadmium exposure groups. The mRNA level of PINK1 was significantly increased, and that of Parkin was decreased in the 48 h cadmium exposure group. Compared to the Cd-exposed group, the Ast group showed more significant improvements in the expression of podocyte structure, functional proteins, and mitochondrial autophagy pathway proteins. The immunological assay of mitochondrial autophagic pathway proteins further indicated that Cd-induced damage to MPC5 cells might be associated with the dysregulation of mitochondrial autophagy.

Innate lymphoid cells (ILCs) develop from ILC progenitors in the bone marrow. Various ILC precursors (ILCPs) with different ILC subset lineage potentials have been identified based on the expression of cell surface markers and ILC-associated key transcription factor reporter genes. This study characterized an interleukin (IL)-7Rα+IL-18Rα+ ILC progenitor population in the mouse bone marrow with multi-ILC lineage potential on the clonal level. Single-cell gene expression analysis revealed the heterogeneity of this population and identified several subpopulations with specific ILC subset-biased gene expression profiles. The role of IL-18 signaling in the regulation of IL-18Rα+ ILC progenitors and ILC development was further investigated using Il18- and Il18r1-deficient mice, in vitro differentiation assay, and adoptive transfer model. IL-18/IL-18R-mediated signal was found to not be required for early stages of ILC development. While Il18r1-/- lymphoid progenitors were able to generate all ILC subsets in vitro and in vivo like the wild-type counterpart, increased IL-18 level, as often occurred during infection or under stress, suppressed the growth of ILCP/ILC in an IL-18Ra-dependent manner via inhibiting proliferation and inducing apoptosis.

The high-glucose-induced cytotoxicity in diabetes has been widely recognized. Staphylococcus aureus is the most frequent pathogen isolated from diabetic foot ulcers, but the properties of this bacterium under high glucose conditions remain unclear. S. aureus grew in medium usually forms weak biofilm, and which was significantly increased by addition of glucose. However, extracellular DNA (eDNA), an important component of biofilms, was markedly decreased in presence of 15 mM glucose. The reduced eDNA content was not caused by degradation, because the nuclease activity of biofilm supernatants with glucose was significantly decreased due to the acidic pH of the medium. Under planktonic state, the growth of S. aureus was significantly decreased in the Luria-Bertani (LB) medium supplemented with 25 mM glucose, and the reduced growth of S. aureus by glucose was dose-dependent. Except for glucose, the growth of planktonic S. aureus was also markedly decreased by fructose or sucrose. Amounts of acid metabolites were produced under high glucose conditions, but the survival of planktonic S. aureus was unaffected by these acidic conditions. Cells of S. aureus from the culture medium with glucose had a thinner cell wall and highly resistant to lysostaphin compared with the bacteria cultured in LB medium. mRNA expression of genes encoding pentaglycine bridges, the substrate of lysostaphin, was significantly decreased in S. aureus by glucose. In addition to S. aureus, the growth of Staphylococcus haemolyticus and Staphylococcus epidermidis was also significantly decreased by an excess of glucose, but strains of Enterococcus faecalis, Escherichia coli, and Pseudomonas aeruginosa were unaffected by glucose. In conclusion, the reduced growth of S. aureus under high glucose conditions is due to impairment of the unique cell-wall structure, pentaglycine bridges.

Acute infection of bovine viral diarrhea virus (BVDV) is associated with immune dysfunction and can cause peripheral blood lymphopenia and lymphocyte apoptosis. Our previous study has confirmed that programmed death-1 (PD-1) blockade inhibits peripheral blood lymphocyte (PBL) apoptosis and restores proliferation and anti-viral immune functions of lymphocytes after BVDV infection in vitro. However, the immunomodulatory effects of PD-1 pathway on major PBL subsets are unclear and their underlying molecular mechanisms need to be further studied. Therefore, in this study, we examined PD-1 expression in bovine PBL subsets after BVDV infection in vitro and analyzed the effects of PD-1 blockade on the apoptosis and proliferation of CD4+ and CD8+ T cells and expression of PD-1 downstream signaling molecules. The results showed that PD-1 expression was enhanced on CD4+ and CD8+ T cells, but not on CD21+ B cells after cytopathic (CP) BVDV (strain NADL) and non-cytopathic (NCP) BVDV (strain KD) infection in vitro and PD-1 blockade significantly reduced the apoptosis of CD4+ and CD8+ T cells after these two strains infection. Remarkably, PD-1 blockade significantly increased the proliferation of CD4+ and CD8+ T cells after CP BVDV infection, but only significantly increased the proliferation of CD4+ T cells after NCP BVDV infection. In addition, we confirmed that PD-1-mediated PI3K/Akt/mTOR, caspase 9/caspase 3 and ERK pathways are involved in regulating the apoptosis and proliferation of CD4+ and CD8+ T cells during BVDV infection in vitro. Notably, ERK is involved in the regulation mechanism PD-1 mediated only when the cells are infected with CP BVDV. Our findings provide a scientific basis for exploring the molecular mechanism of immune dysfunction caused by acute BVDV infection.

MoO3 is now utilized as a promising catalyst due to its high activity and favorable mobility at low temperature. Its spectral data and surface microstructures were characterized by Fourier transform infrared spectra (FT-IR) and Field emission scanning electron microscope (FESEM). Thermo-analysis of the carbon black was performed over nano-MoO3 catalyst in a thermogravimetric analyzer (TGA) at various heating rates and soot-catalyst ratios. Through the analysis of kinetic parameters, we found that the heat transfer effect and diffusion effect can be removed by setting lower heating rates and soot-catalyst ratios. Therefore, a strategy for selecting proper thermogravimetric parameters were established, which can contribute to the better understanding of thermo-analytical process.

The effects of two pilot injections on combustion and emissions were evaluated in a single−cylinder turbocharged diesel engine, which operated in premixed charge compression ignition (PCCI) modes with multiple injections and heavy exhaust gas recirculation under the low load by experiments and simulation. It was revealed that with the delay of the start of the first pilot injection (SOI−P1) or the advance of the start of second pilot injection (SOI−P2), respectively, the pressure, heat release rate (HRR), and temperature peak were all increased. Analysis of the combustion process indicates that, during the two pilot injection periods, the ignition timing was mainly determined by the SOI−P2 while the first released heat peak was influenced by SOI−P1. With the delay of SOI−P1 or the advance of SOI−P2, nitrogen oxide (NOx) generation increased significantly while soot generation varied a little. In addition, increasing Q1 and decreasing the second pilot injection quantity (Q2) can manipulate the NOx and soot at a low level. The advance in SOI−P2 of 5 °CA couple with increasing Q1 and reducing Q2 was proposed, which can mitigate the compromise between emissions and thermal efficiency under the low load in the present PCCI mode.

BackgroundThousands of genetic variants have been associated with hematological traits, though target genes remain unknown at most loci. Moreover, limited analyses have been conducted in African ancestry and Hispanic/Latino populations; hematological trait associated variants more common in these populations have likely been missed.MethodsTo derive gene expression prediction models, we used ancestry-stratified datasets from the Multi-Ethnic Study of Atherosclerosis (MESA, including n = 229 African American and n = 381 Hispanic/Latino participants, monocytes) and the Depression Genes and Networks study (DGN, n = 922 European ancestry participants, whole blood). We then performed a transcriptome-wide association study (TWAS) for platelet count, hemoglobin, hematocrit, and white blood cell count in African (n = 27,955) and Hispanic/Latino (n = 28,324) ancestry participants.ResultsOur results revealed 24 suggestive signals (p < 1 × 10-4) that were conditionally distinct from known GWAS identified variants and successfully replicated these signals in European ancestry subjects from UK Biobank. We found modestly improved correlation of predicted and measured gene expression in an independent African American cohort (the Genetic Epidemiology Network of Arteriopathy (GENOA) study (n = 802), lymphoblastoid cell lines) using the larger DGN reference panel; however, some genes were well predicted using MESA but not DGN.ConclusionsThese analyses demonstrate the importance of performing TWAS and other genetic analyses across diverse populations and of balancing sample size and ancestry background matching when selecting a TWAS reference panel.

Most genome-wide association and fine-mapping studies to date have been conducted in individuals of European descent, and genetic studies of populations of Hispanic/Latino and African ancestry are limited. In addition, these populations have more complex linkage disequilibrium structure. In order to better define the genetic architecture of these understudied populations, we leveraged >100,000 phased sequences available from deep-coverage whole genome sequencing through the multi-ethnic NHLBI Trans-Omics for Precision Medicine (TOPMed) program to impute genotypes into admixed African and Hispanic/Latino samples with genome-wide genotyping array data. We demonstrated that using TOPMed sequencing data as the imputation reference panel improves genotype imputation quality in these populations, which subsequently enhanced gene-mapping power for complex traits. For rare variants with minor allele frequency (MAF) < 0.5%, we observed a 2.3- to 6.1-fold increase in the number of well-imputed variants, with 11-34% improvement in average imputation quality, compared to the state-of-the-art 1000 Genomes Project Phase 3 and Haplotype Reference Consortium reference panels. Impressively, even for extremely rare variants with minor allele count 86%. Subsequent association analyses of TOPMed reference panel-imputed genotype data with hematological traits (hemoglobin (HGB), hematocrit (HCT), and white blood cell count (WBC)) in ~21,600 African-ancestry and ~21,700 Hispanic/Latino individuals identified associations with two rare variants in the HBB gene (rs33930165 with higher WBC [p = 8.8x10-15] in African populations, rs11549407 with lower HGB [p = 1.5x10-12] and HCT [p = 8.8x10-10] in Hispanics/Latinos). By comparison, neither variant would have been genome-wide significant if either 1000 Genomes Project Phase 3 or Haplotype Reference Consortium reference panels had been used for imputation. Our findings highlight the utility of the TOPMed imputation reference panel for identification of novel rare variant associations not previously detected in similarly sized genome-wide studies of under-represented African and Hispanic/Latino populations.

BP180, also termed collagen XVII, is a hemidesmosomal transmembrane glycoprotein expressed in basal keratinocytes, and functions as a cell-matrix adhesion molecule in the dermal-epidermal junction of the skin. Its function, other than cell-matrix adhesion, remains unclear. We generated a mouse strain with BP180 dysfunction (termed ∆NC16A), which develops spontaneous skin inflammation accompanied by an influx of myeloid derived suppressor cells (MDSCs). We used the B16 mouse melanoma model to demonstrate that BP180 dysfunction in either skin or basal keratinocytes promotes MDSC influx into skin and tumor progression. MDSC depletion reduced tumor progression in ∆NC16A mice, demonstrating a critical role for BP180 dysfunction-driven MDSCs in melanoma progression. This study provides the first direct evidence that BP180, a cell-cell matrix adhesion molecule, possesses antitumor function through modulating infiltration of MDSCs. Basal keratinocytes actively participate in skin microenvironment changes caused by BP180 dysfunction. ∆NC16A mice could be a new animal model to study the melanoma microenvironment.

Calcineurin is a serine/threonine protein phosphatase that is highly conserved from yeast to human and plays a critical role in many physiological processes. Regulators of calcineurin (RCANs) are a family of endogenous calcineurin regulators, which are capable of inhibiting the catalytic activity of calcineurin in vivo and in vitro. In this study, we first characterized the biochemical properties of yeast calcineurin and its endogenous regulator Rcn1, a yeast homolog of RCAN1. Our data show that Rcn1 inhibits yeast calcineurin toward pNPP substrate with a noncompetitive mode; and Rcn1 binds cooperatively to yeast calcineurin through multiple low‐affinity interactions at several docking regions. Next, we reinvestigated the mechanism underlying the inhibition of mammalian calcineurin by RCAN1 using a combination of biochemical, biophysical, and computational methods. In contrast to previous observations, RCAN1 noncompetitively inhibits calcineurin phosphatase activity toward both pNPP and phospho‐RII peptide substrates by targeting the enzyme active site in part. Re‐analysis of previously reported kinetic data reveals that the RCAN1 concentrations used were too low to distinguish between the inhibition mechanisms [Chan B et al. (2005) Proc Natl Acad Sci USA 102, 13075]. The results presented in this study provide new insights into the interaction between calcineurin and RCAN1/Rcn1. [ABSTRACT FROM AUTHOR]