Emulsion formation and stabilization by biomolecules: the leading role of cellulose

Emulsion stabilization by native cellulose has been mainly hampered because of its insolubility in water. Chemical modification is normally needed to obtain water-soluble cellulose derivatives. These modified celluloses have been widely used for a range of applications by the food, cosmetic, pharmaceutic, paint and construction industries. In most cases, the modified celluloses are used as rheology modifiers (thickeners) or as emulsifying agents. In the last decade, the structural features of cellulose have been revisited, with particular focus on its structural anisotropy (amphiphilicity) and the molecular interactions leading to its resistance to dissolution. The amphiphilic behavior of native cellulose is evidenced by its capacity to adsorb at the interface between oil and aqueous solvent solutions, thus being capable of stabilizing emulsions. In this overview, the fundamentals of emulsion formation and stabilization by biomolecules are briefly revisited before different aspects around the emerging role of cellulose as emulsion stabilizer are addressed in detail. Particular focus is given to systems stabilized by native cellulose, either molecularly-dissolved or not (Pickering-like effect).Financially support by the Portuguese Foundation for Science and Technology, FCT, via the projects PTDC/AGR-TEC/4814/2014, PTDC/ASP-SIL/30619/2017 and researcher grant IF/01005/2014. RISE Research Institutes of Sweden AB and PERFORM, a competence platform in Formulation Science at RISE, are acknowledged for additional financing. This research has been supported by Treesearch.se.info:eu-repo/semantics/publishedVersio

Veterinarians in the UK on the use of non-steroidal anti-inflammatory drugs (NSAIDs) for post-disbudding analgesia of calves

<p>Top 20 down-regulated genes after DAPT treatment in P0 Lfng-GFP⁺ cells.</p

Sulphate-controlled Diversity of Subterranean Microbial Communities over Depth in Deep Groundwater with Opposing Gradients of Sulphate and Methane

The groundwater system in Olkiluoto, Finland, is stratified with a mixing layer at a depth of approximately 300m between sulphate-rich, methane-poor and sulphate-poor, methane-rich groundwaters. New sequence library data obtained by 454 pyrotag sequencing of the v4v6 16S rDNA region indicated that sulphate-reducing bacteria (SRB) dominated the mixing layer while SRB could not be detected in the deep sulphate-poor groundwater samples. With the indispensable support of the sequence data, it could be demonstrated that sulphate was the only component needed to trigger a very large community transition in deep sulphate-poor, methane-rich groundwater from a non-sulphate-reducing community comprising Hydrogenophaga, Pseudomonas, Thiobacillus, Fusibacter, and Lutibacter to a sulphate-reducing community with Desulfobacula, Desulfovibrio, Desufobulbaceae, Desulfobacterium, Desulfosporosinus, and Desulfotignum. Experiments with biofilms and planktonic microorganisms in flow cells under in situ conditions confirmed that adding sulphate to the sulphate-poor groundwater generated growth of cultivable SRB and detectable SRB-related sequences. It was also found that the 16S rDNA diversity of the biofilms was conserved over 103 d and that there was great similarity in diversity between the microorganisms in the biofilms and in the flowing groundwater. This work demonstrates that the presence/absence of only one geochemical parameter, i.e., sulphate, in the groundwater significantly influenced the diversity of the investigated subterranean microbial community

Multiple functional risk variants in a SMAD7 enhancer implicate a colorectal cancer risk haplotype

Genome-wide association studies (GWAS) of colorectal cancer (CRC) have led to the identification of a number of common variants associated with modest risk. Several risk variants map within the vicinity of TGFβ/BMP signaling pathway genes, including rs4939827 within an intron of SMAD7 at 18q21.1. A previous study implicated a novel SNP (novel 1 or rs58920878) as a functional variant within an enhancer element in SMAD7 intron 4. In this study, we show that four SNPs including novel 1 (rs6507874, rs6507875, rs8085824, and rs58920878) in linkage disequilibrium (LD) with the index SNP rs4939827 demonstrate allele-specific enhancer effects in a large, multi-component enhancer of SMAD7. All four SNPs demonstrate allele-specific protein binding to nuclear extracts of CRC cell lines. Furthermore, some of the risk-associated alleles correlate with increased expression of SMAD7 in normal colon tissues. Finally, we show that the enhancer is responsive to BMP4 stimulation. Taken together, we propose that the associated CRC risk at 18q21.1 is due to four functional variants that regulate SMAD7 expression and potentially perturb a BMP negative feedback loop in TGFβ/BMP signaling pathways

The Oregon Experiment — Effects of Medicaid on Clinical Outcomes

Background: Despite the imminent expansion of Medicaid coverage for low-income adults, the effects of expanding coverage are unclear. The 2008 Medicaid expansion in Oregon based on lottery drawings from a waiting list provided an opportunity to evaluate these effects. Methods: Approximately 2 years after the lottery, we obtained data from 6387 adults who were randomly selected to be able to apply for Medicaid coverage and 5842 adults who were not selected. Measures included blood-pressure, cholesterol, and glycated hemoglobin levels; screening for depression; medication inventories; and self-reported diagnoses, health status, health care utilization, and out-of-pocket spending for such services. We used the random assignment in the lottery to calculate the effect of Medicaid coverage. Results: We found no significant effect of Medicaid coverage on the prevalence or diagnosis of hypertension or high cholesterol levels or on the use of medication for these conditions. Medicaid coverage significantly increased the probability of a diagnosis of diabetes and the use of diabetes medication, but we observed no significant effect on average glycated hemoglobin levels or on the percentage of participants with levels of 6.5% or higher. Medicaid coverage decreased the probability of a positive screening for depression (−9.15 percentage points; 95% confidence interval, −16.70 to −1.60; P=0.02), increased the use of many preventive services, and nearly eliminated catastrophic out-of-pocket medical expenditures. Conclusions: This randomized, controlled study showed that Medicaid coverage generated no significant improvements in measured physical health outcomes in the first 2 years, but it did increase use of health care services, raise rates of diabetes detection and management, lower rates of depression, and reduce financial strain.United States. Dept. of Health and Human Services. Office of the Assistant Secretary for Planning and EvaluationCalifornia HealthCare FoundationNational Institute on Aging (P30AG012810)National Institute on Aging (RC2AGO36631)National Institute on Aging (R01AG0345151)John D. and Catherine T. MacArthur FoundationRobert Wood Johnson FoundationAlfred P. Sloan FoundationSmith Richardson FoundationUnited States. Social Security Administration (5 RRC 08098400-03-00, to the National Bureau of Economic Research as part of the Retirement Research Consortium of the Social Security Administration)Centers for Medicare & Medicaid Services (U.S.

Salt-inducible kinases (SIKs) regulate TGFβ-mediated transcriptional and apoptotic responses

The signalling pathways initiated by members of the transforming growth factor-β (TGFβ) family of cytokines control many metazoan cellular processes, including proliferation and differentiation, epithelial-mesenchymal transition (EMT) and apoptosis. TGFβ signalling is therefore strictly regulated to ensure appropriate context-dependent physiological responses. In an attempt to identify novel regulatory components of the TGFβ signalling pathway, we performed a pharmacological screen by using a cell line engineered to report the endogenous transcription of the TGFβ-responsive target gene PAI-1. The screen revealed that small molecule inhibitors of salt-inducible kinases (SIKs) attenuate TGFβ-mediated transcription of PAI-1 without affecting receptor-mediated SMAD phosphorylation, SMAD complex formation or nuclear translocation. We provide evidence that genetic inactivation of SIK isoforms also attenuates TGFβ-dependent transcriptional responses. Pharmacological inhibition of SIKs by using multiple small-molecule inhibitors potentiated apoptotic cell death induced by TGFβ stimulation. Our data therefore provide evidence for a novel function of SIKs in modulating TGFβ-mediated transcriptional and cellular responses.</p