Cloaking by coating: How effectively does a thin, stiff coating hide a soft substrate?

From human tissue to fruits, many soft materials are coated by a thin layer of a stiffer material. While the primary role of such a coating is often to protect the softer material, the thin, stiff coating also has an important effect on the mechanical behaviour of the composite material, making it appear significantly stiffer than the underlying material. We study this cloaking effect of a coating for the particular case of indentation tests, which measure the `firmness' of the composite solid: we use a combination of theory and experiment to characterize the firmness quantitatively. We find that the indenter size plays a key role in determining the effectiveness of cloaking: small indenters feel a mixture of the material properties of the coating and of the substrate, while large indenters sense largely the unadulterated substrate

Maternal iron deficiency perturbs embryonic cardiovascular development in mice.

Congenital heart disease (CHD) is the most common class of human birth defects, with a prevalence of 0.9% of births. However, two-thirds of cases have an unknown cause, and many of these are thought to be caused by in utero exposure to environmental teratogens. Here we identify a potential teratogen causing CHD in mice: maternal iron deficiency (ID). We show that maternal ID in mice causes severe cardiovascular defects in the offspring. These defects likely arise from increased retinoic acid signalling in ID embryos. The defects can be prevented by iron administration in early pregnancy. It has also been proposed that teratogen exposure may potentiate the effects of genetic predisposition to CHD through gene-environment interaction. Here we show that maternal ID increases the severity of heart and craniofacial defects in a mouse model of Down syndrome. It will be important to understand if the effects of maternal ID seen here in mice may have clinical implications for women

Maternal iron deficiency perturbs embryonic cardiovascular development in mice.

Congenital heart disease (CHD) is the most common class of human birth defects, with a prevalence of 0.9% of births. However, two-thirds of cases have an unknown cause, and many of these are thought to be caused by in utero exposure to environmental teratogens. Here we identify a potential teratogen causing CHD in mice: maternal iron deficiency (ID). We show that maternal ID in mice causes severe cardiovascular defects in the offspring. These defects likely arise from increased retinoic acid signalling in ID embryos. The defects can be prevented by iron administration in early pregnancy. It has also been proposed that teratogen exposure may potentiate the effects of genetic predisposition to CHD through gene-environment interaction. Here we show that maternal ID increases the severity of heart and craniofacial defects in a mouse model of Down syndrome. It will be important to understand if the effects of maternal ID seen here in mice may have clinical implications for women

Specialization along the Left Superior Temporal Sulcus for Auditory Categorization

The affinity and temporal course of functional fields in middle and posterior superior temporal cortex for the categorization of complex sounds was examined using functional magnetic resonance imaging (fMRI) and event-related potentials (ERPs) recorded simultaneously. Data were compared before and after subjects were trained to categorize a continuum of unfamiliar nonphonemic auditory patterns with speech-like properties (NP) and a continuum of familiar phonemic patterns (P). fMRI activation for NP increased after training in left posterior superior temporal sulcus (pSTS). The ERP P2 response to NP also increased with training, and its scalp topography was consistent with left posterior superior temporal generators. In contrast, the left middle superior temporal sulcus (mSTS) showed fMRI activation only for P, and this response was not affected by training. The P2 response to P was also independent of training, and its estimated source was more anterior in left superior temporal cortex. Results are consistent with a role for left pSTS in short-term representation of relevant sound features that provide the basis for identifying newly acquired sound categories. Categorization of highly familiar phonemic patterns is mediated by long-term representations in left mSTS. Results provide new insight regarding the function of ventral and dorsal auditory streams

Overview of Tabletop X-ray Laser Development at the Lawrence Livermore National Laboratory

It is almost a decade since the first tabletop x-ray laser experiments were implemented at the Lawrence Livermore National Laboratory (LLNL). The decision to pursue the picosecond-driven schemes at LLNL was largely based around the early demonstration of the tabletop Ne-like Ti x-ray laser at the Max Born Institute (MBI) as well as the established robustness of collisional excitation schemes. These picosecond x-ray lasers have been a strong growth area for x-ray laser research. Rapid progress in source development and characterization has achieved ultrahigh peak brightness rivaling the previous activities on the larger facilities. Various picosecond soft-x-ray based applications have benefited from the increased repetition rates. We will describe the activities at LLNL in this area

Maternal iron deficiency perturbs embryonic cardiovascular development in mice

Funder: Novo Nordisk; doi: https://doi.org/10.13039/501100004191Funder: National Heart Foundation of Australia (Heart Foundation); doi: https://doi.org/10.13039/501100001030Funder: NSW Health; doi: https://doi.org/10.13039/501100009287Funder: Oxford University | John Fell Fund, University of Oxford (John Fell OUP Research Fund); doi: https://doi.org/10.13039/501100004789Funder: The Federated FoundationAbstract: Congenital heart disease (CHD) is the most common class of human birth defects, with a prevalence of 0.9% of births. However, two-thirds of cases have an unknown cause, and many of these are thought to be caused by in utero exposure to environmental teratogens. Here we identify a potential teratogen causing CHD in mice: maternal iron deficiency (ID). We show that maternal ID in mice causes severe cardiovascular defects in the offspring. These defects likely arise from increased retinoic acid signalling in ID embryos. The defects can be prevented by iron administration in early pregnancy. It has also been proposed that teratogen exposure may potentiate the effects of genetic predisposition to CHD through gene–environment interaction. Here we show that maternal ID increases the severity of heart and craniofacial defects in a mouse model of Down syndrome. It will be important to understand if the effects of maternal ID seen here in mice may have clinical implications for women