A corrected formula for uncertainty in estimations of gestational age from fetal head circumference measurements

Numerous publications over recent years have proposed methods for estimation of gestational age (GA) from fetal measurements including biparietal diameter, head circumference, crown-rump length and others. The manuscript of Altman and Chitty1 presented statistical modelling of data from 663 fetuses to define charts and tables for pregnancy dating based upon such measures. The resulting outputs are tables of mean GA estimates based upon each measurement, each with a corresponding standard deviation that encompasses the uncertainty in the prediction. We here address an erroneous result in the appendix of this work, associated with the uncertainty in GA prediction based upon derived head circumference measurements

Buckling of a growing tissue and the emergence of two-dimensional patterns

The process of biological growth and the associated generation of residual stress has previously been considered as a driving mechanism for tissue buckling and pattern selection in numerous areas of biology. Here, we develop a two-dimensional thin plate theory to simulate the growth of cultured intestinal epithelial cells on a deformable substrate, with the goal of elucidating how a tissue engineer might best recreate the regular array of invaginations (crypts of Lieberkühn) found in the wall of the mammalian intestine. We extend the standard von Kármán equations to incorporate inhomogeneity in the plate’s mechanical properties and surface stresses applied to the substrate by cell proliferation. We determine numerically the configurations of a homogeneous plate under uniform cell growth, and show how tethering to an underlying elastic foundation can be used to promote higher-order buckled configurations. We then examine the independent effects of localised softening of the substrate and spatial patterning of cellular growth, demonstrating that (within a two-dimensional framework, and contrary to the predictions of one-dimensional models) growth patterning constitutes a more viable mechanism for control of crypt distribution than does material inhomogeneity

Biogeochemical Changes During Bio-cementation Mediated by Stimulated and Augmented Ureolytic Microorganisms.

Microbially Induced Calcite Precipitation (MICP) is a bio-mediated cementation process that can improve the engineering properties of granular soils through the precipitation of calcite. The process is made possible by soil microorganisms containing urease enzymes, which hydrolyze urea and enable carbonate ions to become available for precipitation. While most researchers have injected non-native ureolytic bacteria to complete bio-cementation, enrichment of native ureolytic microorganisms may enable reductions in process treatment costs and environmental impacts. In this study, a large-scale bio-cementation experiment involving two 1.7-meter diameter tanks and a complementary soil column experiment were performed to investigate biogeochemical differences between bio-cementation mediated by either native or augmented (Sporosarcina pasteurii) ureolytic microorganisms. Although post-treatment distributions of calcite and engineering properties were similar between approaches, the results of this study suggest that significant differences in ureolysis rates and related precipitation rates between native and augmented microbial communities may influence the temporal progression and spatial distribution of bio-cementation, solution biogeochemical changes, and precipitate microstructure. The role of urea hydrolysis in enabling calcite precipitation through sustained super-saturation following treatment injections is explored

Mr. and Mrs. T. Nelson to James Meredith (Undated)

https://egrove.olemiss.edu/mercorr_pro/1908/thumbnail.jp

Mechanisms and points of control in the spread of inflammation: a mathematical investigation

Understanding the mechanisms that control the body’s response to inflammation is of key importance, due to its involvement in myriad medical conditions, including cancer, arthritis, Alzheimer’s disease and asthma. While resolving inflammation has historically been considered a passive process, since the turn of the century the hunt for novel therapeutic interventions has begun to focus upon active manipulation of constituent mechanisms, particularly involving the roles of apoptosing neutrophils, phagocytosing macrophages and anti-inflammatory mediators. Moreover, there is growing interest in how inflammatory damage can spread spatially due to the motility of inflammatory mediators and immune cells. For example, impaired neutrophil chemotaxis is implicated in causing chronic inflammation under trauma and in ageing, while neutrophil migration is an attractive therapeutic target in ailments such as chronic obstructive pulmonary disease. We extend an existing homogeneous model that captures interactions between inflammatory mediators, neutrophils and macrophages to incorporate spatial behaviour. Through bifurcation analysis and numerical simulation, we show that spatially inhomogeneous outcomes can present close to the switch from bistability to guaranteed resolution in the corresponding homogeneous model. Finally, we show how aberrant spatial mechanisms can play a role in the failure of inflammation to resolve and discuss our results within the broader context of seeking novel inflammatory treatments