Financial mathematics of bankers’ practice

This study aims to present financial mathematics that bankers use in their practice when they are embedded in their workplace. To that end, we observed bankers at two official banks in an inland city of Brazil. Our analysis reveals that financial mathematics actions are structured by banking systems; the actions linked to these systems are characterised by the ways the bankers address the opportunities and limitations of banking systems as cultural tools that serve as a unit of analysis and define specific actions in this context. However, at the same time, it illustrates cases where bankers deal with some limitations of the systems. In other words, while their actions are mediated by these systems, some bankers deliver customer service by considering the customer's specific situation and profile in the decision-making process, thus providing a service that the system alone cannot do

Exploring the relative value of end of life QALYs: are the comparators important?

In the UK, life extending, end-of-life (EoL) treatments are an exception to standard cost-per-quality-adjusted life year (QALY) thresholds. This implies that greater value is placed on gaining these QALYs, than QALYs gained by the majority of other patient groups treated for anything else in the health system, even for other EoL contexts (such as quality of life (QoL) improvements alone). This paper reports a Person Trade-Off (PTO) study to test whether studies that find societal support for prioritising EoL life extensions can be explained by the severity, in terms of prospective QALYs loss, of the non-terminal comparator scenarios. Eight health scenarios were designed depicting i) QoL improvements for non-EoL temporary (T-QoL) and chronic (C-QoL) health problems and ii) QoL improvements and life extensions (LEs) for EoL health problems. Preferences were elicited from a quota sample of 901 Scottish respondents in 2016 using PTO techniques via Computer Assisted Personal Interview (CAPI). Our results indicate that there is little evidence to suggest that the severity of non-EoL comparator scenarios influence preferences for EoL treatments. Respondents do not appear to have a preference for EoL over non-EoL health gains; instead there is some indication that non-EoL health gains are preferred, particularly when compared to EoL-LE health gains. Comparing between QoL and life extending EoL scenarios, our results suggest QoL improvements are preferred to life extensions. Overall, results challenge current UK EoL policy which gives additional weight to EoL health gains, particularly EoL life extensions in the case of the National Institute for Health and Care Excellence (NICE)

Chronic inflammation does not mediate the effect of adiposity on grip strength: results from a multivariable Mendelian randomization study

The relationship between adiposity and grip strength (GS) is complex. We investigated whether one pathway through which adiposity affects GS was via chronic inflammation. 367,583 UK Biobank participants had body mass index (BMI), waist-hip-ratio (WHR), C-reactive protein (CRP) and GS data. Univariable Mendelian randomization (MR) and multivariable Mendelian randomization (MVMR) analyses (using inverse variance weighted (IVW) weighted median estimates (WME) and MR-Egger models) estimated total, direct and indirect effects of adiposity traits on GS using genetic instruments for BMI and WHR (exposures) and CRP (mediator). Observational findings suggested higher BMI was associated with stronger grip, e.g., in males, per standard deviation (SD) higher BMI, GS was higher by 0.48 kg (95% confidence interval(CI):0.44,0.51), independent of CRP. For males MR estimates were directionally consistent; for females, estimates were consistent with the null. Observational findings for WHR suggested that higher WHR was associated with weaker grip. In multivariable MR-IVW analyses, effects in males were consistent with the null. In females, there were consistent effects such that higher WHR was associated with stronger grip, e.g., 1-SD higher WHR was associated with 1.25 kg (MVMR-Egger; 95% CI:0.72,1.78) stronger grip, independent of CRP. Across sexes and adiposity indicators, CRP’s mediating role was minor. Greater adiposity may increase GS in early old age, but effects vary by sex and adiposity location. There was no evidence that inflammation mediated these effects

Maternal weight status before pregnancy is strongly associated with offspring weight status in childhood

Commentary on: Heslehurst N, Vieira R, Akhter Z, et al. The association between maternal body mass index and child obesity: a systematic review and meta-analysis. PLoS Medicine 2019;16:e1002817. doi: 10.1371/journal.pmed.1002817

Modeling the Effects of Hyaluronic Acid Degradation on the Regulation of Human Astrocyte Phenotype Using Multicomponent Interpenetrating Polymer Networks (mIPNs)

Hyaluronic acid (HA) is a highly abundant component in the extracellular matrix (ECM) and a fundamental element to the architecture and the physiology of the central nervous system (CNS). Often, HA degradation occurs when an overreactive inflammatory response, derived from tissue trauma or neurodegenerative diseases such as Alzheimer’s, causes the ECM in the CNS to be remodeled. Herein, we studied the effects of HA content as a key regulator of human astrocyte (HAf) reactivity using multicomponent interpenetrating polymer networks (mIPNs) comprised of Collagen I, HA and poly(ethylene glycol) diacrylate. The selected platform facilities the modulation of HA levels independently of matrix rigidity. Total astrocytic processes length, number of endpoints, the expression of the quiescent markers: Aldehyde Dehydrogenase 1 Family Member L1 (ALDH1L1) and Glutamate Aspartate Transporter (GLAST); the reactive markers: Glial Fibrillary Acidic Protein (GFAP) and S100 Calcium-Binding Protein β (S100β); and the inflammatory markers: Inducible Nitric Oxide Synthase (iNOS), Interleukin 1β (IL-1β) and Tumor Necrosis Factor Alpha (TNFα), were assessed. Cumulatively, our results demonstrated that the decrease in HA concentration elicited a reduction in the total length of astrocytic processes and an increase in the expression of HAf reactive and inflammatory markers

Sulfite reduction in mycobacteria

Mycobacterium tuberculosis places an enormous burden on the welfare of humanity. Its ability to grow and its pathogenicity are linked to sulfur metabolism, which is considered a fertile area for the development of antibiotics, particularly because many of the sulfur acquisition steps in the bacterium are not found in the host. Sulfite reduction is one such mycobacterium-specific step and is the central focus of this paper. Sulfite reduction in Mycobacterium smegmatis was investigated using a combination of deletion mutagenesis, metabolite screening, complementation, and enzymology. The initial rate parameters for the purified sulfite reductase from M. tuberculosis were determined under strict anaerobic conditions [kcat = 1.0 (±0.1) electron consumed per second, and Km(SO3−2) = 27 (±1) μM], and the enzyme exhibits no detectible turnover of nitrite, which need not be the case in the sulfite/nitrite reductase family. Deletion of sulfite reductase (sirA, originally misannotated nirA) reveals that it is essential for growth on sulfate or sulfite as the sole sulfur source and, further, that the nitrite-reducing activities of the cell are incapable of reducing sulfite at a rate sufficient to allow growth. Like their nitrite reductase counterparts, sulfite reductases require a siroheme cofactor for catalysis. Rv2393 (renamed che1) resides in the sulfur reduction operon and is shown for the first time to encode a ferrochelatase, a catalyst that inserts Fe2+ into siroheme. Deletion of che1 causes cells to grow slowly on metabolites that require sulfite reductase activity. This slow-growth phenotype was ameliorated by optimizing growth conditions for nitrite assimilation, suggesting that nitrogen and sulfur assimilation overlap at the point of ferrochelatase synthesis and delivery