Ideology and culture

This chapter evaluates the role of culture and ideology in relation to journalism. Journalists cannot ignore that they are not operating in a vacuum, immune to environmental influences. A “western” (or any ideological) approach to journalism is not a neutral norm to which others need to adhere. Journalists can keep themselves and each other in check by questioning the approach taken to a story and identifying the lens they employ. Secondly, diverse recruitment within media organisations is key, not just in terms of ethnic, gender or national backgrounds but also in terms of value profiles. There is no one Nation which holds the gold standard for journalism and can be used as a reference point for all others. In other words, there is no such thing as Greenwich Mean Time journalism

The role of charge-matching in nanoporous materials formation

Unravelling the molecular-level mechanisms that lead to the formation of mesoscale-ordered porous materials is a crucial step towards the goal of computational material design. For silica templated by alkylamine surfactants, a mechanism based on hydrogen-bond interactions between neutral amines and neutral silicates in solution has been widely accepted by the materials science community, despite the lack of conclusive evidence to support it. We demonstrate, through a combination of experimental measurements and multi-scale modelling, that the so-called “neutral templating route” does not represent a viable description of the synthesis mechanism of hexagonal mesoporous silica (HMS), the earliest example of amine-templated porous silica. Instead, the mesoscale structure of the material is defined by charge-matching of ionic interactions between amines and silicates. This has profound implications for the synthesis of a wide range of templated porous materials, and may shed new light on developing sustainable and economical routes to high value porous materials

Towards sex-specific osteoarthritis risk models: evaluation of risk factors for knee osteoarthritis in males and females

Objectives The aim of this study was to identify sex-specific prevalence and strength of risk factors for the incidence of radiographic knee OA (incRKOA). Methods Our study population consisted of 10 958 Rotterdam Study participants free of knee OA in one or both knees at baseline. One thousand and sixty-four participants developed RKOA after a median follow-up time of 9.6 years. We estimated the association between each available risk factor and incRKOA using sex stratified multivariate regression models with generalized estimating equations. Subsequently, we statistically tested sex differences between risk estimates and calculated the population attributable fractions (PAFs) for modifiable risk factors. Results The prevalence of the investigated risk factors was, in general, higher in women compared with men, except that alcohol intake and smoking were higher in men and high BMI showed equal prevalence. We found significantly different risk estimates between men and women: high level of physical activity [relative risk (RR) 1.76 (95% CI: 1.29–2.40)] or a Kellgren and Lawrence score 1 at baseline [RR 5.48 (95% CI: 4.51–6.65)] was higher in men. Among borderline significantly different risk estimates was BMI ≥27, associated with higher risk for incRKOA in women [RR 2.00 (95% CI: 1.74–2.31)]. The PAF for higher BMI was 25.6% in women and 19.3% in men. Conclusion We found sex-specific differences in both presence and relative risk of several risk factors for incRKOA. Especially BMI, a modifiable risk factor, impacts women more strongly than men. These risk factors can be used in the development of personalized prevention strategies and in building sex-specific prediction tools to identify high risk profile patients

The extent of counterion dissociation at the interface of cationic diblock copolymer nanoparticles in non-polar solvents

Hypothesis Diblock copolymer nanoparticles prepared in non-polar solvents that are sterically stabilized but possess ionic functionality from the inclusion of cationic comonomers in the stabilizer shell are known to exhibit complex electrokinetic behavior (Chem. Sci. 9 (2018) 922–934). For example, core-shell nanoparticles with cationic comonomers located solely within the shell layer have lower magnitude electrophoretic mobilities than nanoparticles containing the same cationic comonomers located within the core, and nanoparticles prepared using a minor fraction of steric stabilizer chains containing cationic comonomer repeat units have comparable electrophoretic mobilities to nanoparticles prepared with this cationic comonomer solely located within the core. We hypothesize that these observations can be explained in terms of the strength of the Coulombic interaction between counterions and the nanoparticle interface. Experiments The highly-fluorinated anionic counterion associated with these cationic nanoparticles is studied by 19F nuclear magnetic resonance (NMR) spectroscopy in n-dodecane. This revealed only one type of 19F environment for a soluble macromolecular cation (the oil-soluble steric stabilizer chains used to prepare the nanoparticles), whereas two distinct environments were observed for the sterically-stabilized cationic nanoparticles. Both 19F diffusion NMR and 19F–13C heteronuclear single quantum correlation (HSQC) measurements support the existence of two environments for this counterion. Findings The existence of two distinct 19F environments for the highly-fluorinated anion associated with the sterically-stabilized nanoparticles demonstrates the presence of spectroscopically distinguishable populations of ion pairs and of fully dissociated free anions. 19F NMR spectra recorded for sterically-stabilized nanoparticles with a fully ionic shell (all stabilizer chains containing the cationic comonomer) and those with a partly ionic shell (10% of stabilizer chains containing the cationic comonomer) reveal a higher proportion of dissociated anions in the partly ionic case. This suggests a stronger Coulombic interaction between counterions and the cationic interface when the shell is fully ionic, which accounts for the observed reduction in the magnitude of the electrophoretic mobility

Sepsis is associated with mitochondrial DNA damage and a reduced mitochondrial mass in the kidney of patients with sepsis-AKI

BACKGROUND: Sepsis is a life-threatening condition accompanied by organ dysfunction subsequent to a dysregulated host response to infection. Up to 60% of patients with sepsis develop acute kidney injury (AKI), which is associated with a poor clinical outcome. The pathophysiology of sepsis-associated AKI (sepsis-AKI) remains incompletely understood, but mitochondria have emerged as key players in the pathogenesis. Therefore, our aim was to identify mitochondrial damage in patients with sepsis-AKI. METHODS: We conducted a clinical laboratory study using "warm" postmortem biopsies from sepsis-associated AKI patients from a university teaching hospital. Biopsies were taken from adult patients (n = 14) who died of sepsis with AKI at the intensive care unit (ICU) and control patients (n = 12) undergoing tumor nephrectomy. To define the mechanisms of the mitochondrial contribution to the pathogenesis of sepsis-AKI, we explored mRNA and DNA expression of mitochondrial quality mechanism pathways, DNA oxidation and mitochondrial DNA (mtDNA) integrity in renal biopsies from sepsis-AKI patients and control subjects. Next, we induced human umbilical vein endothelial cells (HUVECs) with lipopolysaccharide (LPS) for 48 h to mimic sepsis and validate our results in vitro. RESULTS: Compared to control subjects, sepsis-AKI patients had upregulated mRNA expression of oxidative damage markers, excess mitochondrial DNA damage and lower mitochondrial mass. Sepsis-AKI patients had lower mRNA expression of mitochondrial quality markers TFAM, PINK1 and PARKIN, but not of MFN2 and DRP1. Oxidative DNA damage was present in the cytosol of tubular epithelial cells in the kidney of sepsis-AKI patients, whereas it was almost absent in biopsies from control subjects. Oxidative DNA damage co-localized with both the nuclei and mitochondria. Accordingly, HUVECs induced with LPS for 48 h showed an increased mnSOD expression, a decreased TFAM expression and higher mtDNA damage levels. CONCLUSION: Sepsis-AKI induces mitochondrial DNA damage in the human kidney, without upregulation of mitochondrial quality control mechanisms, which likely resulted in a reduction in mitochondrial mass

Rectification of thermal fluctuations in ideal gases

We calculate the systematic average speed of the adiabatic piston and a thermal Brownian motor, introduced in [Van den Broeck, Kawai and Meurs, \emph{Microscopic analysis of a thermal Brownian motor}, to appear in Phys. Rev. Lett.], by an expansion of the Boltzmann equation and compare with the exact numerical solution.Comment: 18 page

Effects of Early IL-17A Neutralization on Disease Induction in a Primate Model of Experimental Autoimmune Encephalomyelitis

We report on the effect of antibody-mediated neutralization of interleukin (IL)-17A in a non-human primate experimental autoimmune encephalomyelitis (EAE) model induced with recombinant human myelin oligodendrocyte glycoprotein (rhMOG). We tested a human-anti-human IL-17A-antibody in two doses (3 and 30 mg/kg) against placebo (PBS). The treatment was started 1 day before EAE induction and continued throughout the experiment. Although all monkeys developed clinically evident EAE, the onset of neurological signs was delayed in some monkeys from both treatment groups. Total CNS lesion volumes, demyelination, or inflammation did not differ between the different groups. Immune profiling revealed an altered distribution of IL-17A producing cells in the lymphoid organs of antibody-treated monkeys. Comparable numbers of IL-17A producing cells were observed in the brain. RhMOG-induced T cell proliferation in the lymph nodes was slightly reduced after anti-IL-17A antibody treatment. To summarize, we found that anti-IL-17A antibody as a single treatment from disease induction effects a trend towards delayed neurological disease progression in the marmoset EAE model, although the effect did not reach statistical significance. This suggests a role of IL-17A in late stage disease in the marmoset EAE model, but IL-17A may not be the dominant pathogenic cytokine

The contribution of hip geometry to the prediction of hip osteoarthritis

SummaryObjectiveTo determine how well measures of hip geometry can predict radiological incident hip osteoarthritis (HOA) compared to well known clinical risk factors.DesignThe study population is part of the Rotterdam Study, a prospective population-based cohort. Baseline pelvic radiographs were used to measure hip geometry by two methods: Statistical Shape Models (SSM) and predefined geometry parameters (PGPs). Incident HOA (Kellgren and Lawrence (KL) ≥ 2) was assessed in 688 participants after 6.5 years without radiographic HOA at baseline. The ability to predict HOA was quantified using the area under the Receiver Operating Characteristics (ROC) curve (AUC).ResultsComparison of the two methods showed that both contain information that is not captured by the other method. At 6.5 years follow-up 132 hips had incident HOA. Five PGPs (Wiberg angle, Neck Width (NW), Pelvic Width (PW), Hip Axis Length (HAL) and Triangular Index (TI)) and two SSM (modes 5 and 9) were significant predictors of HOA (P = 0.007). Hip geometry added 7% to the prediction obtained by clinical risk factors (AUC = 0.67 (geometry), 0.66 (gender, age, Body Mass Index (BMI)) and combining both: AUC = 0.73, respectively). Mode 12 (associated with position of the femoral head in acetabulum) and Wiberg angle were predictors of HOA in participants without radiological signs at baseline (KL = 0). Although the strength of the prediction decreased for all variables at a longer follow-up, the contribution of hip geometry was still significant (P = 0.01).ConclusionsHip geometry has a moderate ability to predict HOA in participants with and without initial signs of osteoarthritis (OA), similar to and largely independent of the predictive value of clinical risk factors