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The pH value of oil acidized wastewater is relatively low (pH = 6.1), which seriously affects the flocculation of polyacrylamide (PAM). NaOH was used to adjust the pH value, but the maximum was only 7.5. The regulation was limited as the Ca2þ in aqueous phase up to 1,350 mg L-1 consumed OH-. A novel formulation of Na2CO3 þ PAM was proposed to form CaCO3 floc core to facilitate PAM coagulation. When the concentration was above 400 mg L-1, the PAM precipitation tended to be maximum, followed by NaOH adjustment of pH to 8.0 that could enhance PAM flocculation successively. The sewage sludge (SS) remained and residue oil reduced to 25 mg L-1 and 34 mg L-1 respectively. The analysis of the species and composition of fatty acids indicated that the coagulation-flocculation selectively effected the sedimentation of saturated fatty acids (SAT). This provides a new idea for recovery of high value-added residual oil. The optimal additive of Na2CO3 is expected as promising coagulant aid to improve the PAM coagulation-flocculation of oil acidized wastewater. [ABSTRACT FROM AUTHOR]

We evaluated in vivo innate immune responses in monocyte populations from 67 young (aged 21-30 years) and older (aged ≥65 years) adults before and after influenza vaccination. CD14+CD16+ inflammatory monocytes were induced after vaccination in both young and older adults. In classical CD14+CD16- and inflammatory monocytes, production of tumor necrosis factor α and interleukin 6, as measured by intracellular staining, was strongly induced after vaccination. Cytokine production was strongly associated with influenza vaccine antibody response; the highest levels were found as late as day 28 after vaccination in young subjects and were substantially diminished in older subjects. Notably, levels of the anti-inflammatory cytokine interleukin 10 (IL-10) were markedly elevated in monocytes from older subjects before and after vaccination. In purified monocytes, we found age-associated elevation in phosphorylated signal transducer and activator of transcription-3, and decreased serine 359 phosphorylation of the negative IL-10 regulator dual-specificity phosphatase 1. These findings for the first time implicate dysregulated IL-10 production in impaired vaccine responses in older adults. [ABSTRACT FROM AUTHOR]

NLRs (nucleotide-binding domain leucine-rich-repeat-containing receptors; NOD-like receptors) are a class of pattern recognition receptor (PRR) that respond to host perturbation from either infectious agents or cellular stress1,2. The function of most NLR family members has not been characterized and their role in instructing adaptive immune responses remains unclear2,3. NLRP10 (also known as PYNOD, NALP10, PAN5 and NOD8) is the only NLR lacking the putative ligand-binding leucine-rich-repeat domain, and has been postulated to be a negative regulator of other NLR members, including NLRP3 (refs 4–6). We did not find evidence that NLRP10 functions through an inflammasome to regulate caspase-1 activity nor that it regulates other inflammasomes. Instead, Nlrp10−/− mice had a profound defect in helper T-cell-driven immune responses to a diverse array of adjuvants, including lipopolysaccharide, aluminium hydroxide and complete Freund’s adjuvant. Adaptive immunity was impaired in the absence of NLRP10 because of a dendritic cell (DC) intrinsic defect in emigration from inflamed tissues, whereas upregulation of DC costimulatory molecules and chemotaxis to CCR7-dependent and -independent ligands remained intact. The loss of antigen transport to the draining lymph nodes by a subset of migratory DCs resulted in an almost absolute loss in naive CD4+ T-cell priming, highlighting the critical link between diverse innate immune stimulation, NLRP10 activity and the immune function of mature DCs. [ABSTRACT FROM AUTHOR]

Background: High-throughput DNA methylation arrays are likely to accelerate the pace of methylation biomarker discovery for a wide variety of diseases. A potential problem with a standard set of probes measuring the methylation status of CpG sites across the whole genome is that many sites may not show inter-individual methylation variation among the biosamples for the disease outcome being studied. Inclusion of these so-called "non-variable sites" will increase the risk of false discoveries and reduce statistical power to detect biologically relevant methylation markers. Results: We propose a method to estimate the proportion of non-variable CpG sites and eliminate those sites from further analyses. Our method is illustrated using data obtained by hybridizing DNA extracted from the peripheral blood mononuclear cells of 311 samples to an array assaying 1505 CpG sites. Results showed that a large proportion of the CpG sites did not show inter-individual variation in methylation. Conclusions: Our method resulted in a substantial improvement in association signals between methylation sites and outcome variables while controlling the false discovery rate at the same level. [ABSTRACT FROM AUTHOR]

Summary: BLISS 2.0 is a web-based application for identifying conserved regulatory modules in distantly related orthologous sequences. Unlike existing approaches, it performs the cross-genome comparison at the binding site level. Experimental results on simulated and real world data indicate that BLISS 2.0 can identify conserved regulatory modules from sequences with little overall similarity at the DNA sequence level. Availability: http://www.blisstool.org/ Contact: leizhou@ufl.edu [ABSTRACT FROM AUTHOR]