The burden of childhood atopic dermatitis in the primary care setting: a report from the Meta-LARC Consortium

Background: Little is known about the burden of AD encountered in U.S. primary care practices and the frequency and type of skin care practices routinely used in children. Objectives: To estimate the prevalence of AD and allergic comorbidities in children 0-5 years attending primary care practices in the U.S. and to describe routine skin care practices used in this population. Design: A cross-sectional survey study of a convenience sample of children under the age of 5 attending primary care practices for any reason. Setting: Ten primary care practices in five U.S. states.Results: Amongst 652 children attending primary care practices, the estimated prevalence of ever having AD was 24 % (95% CI= 21-28) ranging from 15% among those under the age of one to 38% among those aged 4- 5 years. The prevalence of comorbid asthma was higher among AD participants compared to those with no AD, 12% and 4%, respectively (p less than 0.001). Moisturizers with high water:oil ratios were most commonly used (i.e., lotions) in the non-AD population, whereas moisturizers with low water:oil content (i.e. ointments) most common when AD was present. Conclusions: Our study found a large burden of AD in the primary care practice setting in the U.S. The majority of households reported skin care practices in children without AD that may be detrimental to the skin barrier such as frequent bathing and the routine use of moisturizers with high water: oil ratios. Clinical trials are needed to identify which skin care practices are optimal for reducing the significant risk of AD in the community

Reconciling global-model estimates and country reporting of anthropogenic forest CO2 sinks

This is the author accepted manuscript. The final version is available from Springer Nature via the DOI in this recordData availability: The data that support the findings of this study are available from the corresponding author upon request.Achieving the long-term temperature goal of the Paris Agreement requires forest-based mitigation. Collective progress towards this goal will be assessed by the Paris Agreement’s Global stocktake. At present, there is a discrepancy of about 4 GtCO2yr−1in global anthropogenic net land-use emissions between global models (reflected in IPCC assessment reports) and aggregated national GHG inventories (under the UNFCCC). We show that a substantial part of this discrepancy (about 3.2 GtCO2yr−1) can be explained by conceptual differences in anthropogenic forest sink estimation, related to the representation of environmental change impacts and the areas considered as managed. For a more credible tracking of collective progress under the Global stocktake, these conceptual differences between models and inventories need to be reconciled. We implement a new method of disaggregation of global land model results that allows greater comparability with GHG inventories. This provides a deeper understanding of model–inventory differences, allowing more transparent analysis of forest-based mitigation and facilitating a more accurate Global stocktake.J.H. was supported by EU FP7 through project LUC4C (GA603542) and the UK NERC project GGRiLS-GAP. G.G. was supported by Administrative Arrangement Number 340203/2016/742550/SER/CLIMA.A3. A.K.J. was supported by the NSF (AGS 12-43071) and DOE (DE-SC0016323). J.E.M.S.N. was supported by the German Research Foundation’s Emmy Noether Programme (grant number PO1751/1-1). G.G., J.H., G.P.P. and L.P. received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement number 776810 (VERIFY). C.D.K. was supported by the US DOE under Contract DE-AC02-05CH11231 as part of their RGMA (BGC-Feedbacks SFA) and TES Programs (NGEE-Tropics). A.K.J. was supported under the US NSF (NSF-AGS-12-43071)

Epigenetic reprogramming of breast cancer cells with oocyte extracts

<p>Abstract</p> <p>Background</p> <p>Breast cancer is a disease characterised by both genetic and epigenetic alterations. Epigenetic silencing of tumour suppressor genes is an early event in breast carcinogenesis and reversion of gene silencing by epigenetic reprogramming can provide clues to the mechanisms responsible for tumour initiation and progression. In this study we apply the reprogramming capacity of oocytes to cancer cells in order to study breast oncogenesis.</p> <p>Results</p> <p>We show that breast cancer cells can be directly reprogrammed by amphibian oocyte extracts. The reprogramming effect, after six hours of treatment, in the absence of DNA replication, includes DNA demethylation and removal of repressive histone marks at the promoters of tumour suppressor genes; also, expression of the silenced genes is re-activated in response to treatment. This activity is specific to oocytes as it is not elicited by extracts from ovulated eggs, and is present at very limited levels in extracts from mouse embryonic stem cells. Epigenetic reprogramming in oocyte extracts results in reduction of cancer cell growth under anchorage independent conditions and a reduction in tumour growth in mouse xenografts.</p> <p>Conclusions</p> <p>This study presents a new method to investigate tumour reversion by epigenetic reprogramming. After testing extracts from different sources, we found that axolotl oocyte extracts possess superior reprogramming ability, which reverses epigenetic silencing of tumour suppressor genes and tumorigenicity of breast cancer cells in a mouse xenograft model. Therefore this system can be extremely valuable for dissecting the mechanisms involved in tumour suppressor gene silencing and identifying molecular activities capable of arresting tumour growth. These applications can ultimately shed light on the contribution of epigenetic alterations in breast cancer and advance the development of epigenetic therapies.</p

Metformin Represses Self-Renewal of the Human Breast Carcinoma Stem Cells via Inhibition of Estrogen Receptor-Mediated OCT4 Expression

Metformin, a Type II diabetic treatment drug, which inhibits transcription of gluconeogenesis genes, has recently been shown to lower the risk of some diabetes-related tumors, including breast cancer. Recently, “cancer stem cells” have been demonstrated to sustain the growth of tumors and are resistant to therapy. To test the hypothesis that metformin might be reducing the risk to breast cancers, the human breast carcinoma cell line, MCF-7, grown in 3-dimensional mammospheres which represent human breast cancer stem cell population, were treated with various known and suspected breast cancer chemicals with and without non-cytotoxic concentrations of metformin. Using OCT4 expression as a marker for the cancer stem cells, the number and size were measured in these cells. Results demonstrated that TCDD (100 nM) and bisphenol A (10 µM) increased the number and size of the mammospheres, as did estrogen (10 nM E2). By monitoring a cancer stem cell marker, OCT4, the stimulation by these chemicals was correlated with the increased expression of OCT4. On the other hand, metformin at 1 and 10 mM concentration dramatically reduced the size and number of mammospheres. Results also demonstrated the metformin reduced the expression of OCT4 in E2 & TCDD mammospheres but not in the bisphenol A mammospheres, suggesting different mechanisms of action of the bisphenol A on human breast carcinoma cells. In addition, these results support the use of 3-dimensional human breast cancer stem cells as a means to screen for potential human breast tumor promoters and breast chemopreventive and chemotherapeutic agents

Lower land-use emissions responsible for increased net land carbon sink during the slow warming period

The terrestrial carbon sink accelerated during 1998–2012, concurrently with the slow warming period, but the mechanisms behind this acceleration are unclear. Here we analyse recent changes in the net land carbon sink (NLS) and its driving factors, using atmospheric inversions and terrestrial carbon models. We show that the linear trend of NLS during 1998–2012 is about 0.17 ± 0.05 Pg C yr−2 , which is three times larger than during 1980–1998 (0.05 ± 0.05 Pg C yr−2). According to terrestrial carbon model simulations, the intensification of the NLS cannot be explained by CO2 fertilization or climate change alone. We therefore use a bookkeeping model to explore the contribution of changes in land-use emissions and find that decreasing land-use emissions are the dominant cause of the intensification of the NLS during the slow warming period. This reduction of land-use emissions is due to both decreased tropical forest area loss and increased afforestation in northern temperate regions. The estimate based on atmospheric inversions shows consistently reduced land-use emissions, whereas another bookkeeping model did not reproduce such changes, probably owing to missing the signal of reduced tropical deforestation. These results highlight the importance of better constraining emissions from land-use change to understand recent trends in land carbon sinks

ECG-gated interventional cardiac reconstruction for non-periodic motion

Abstract. The 3-D reconstruction of cardiac vasculature using C-arm CT is an active and challenging field of research. In interventional environments patients often do have arrhythmic heart signals or cannot hold breath during the complete data acquisition. This important group of patients cannot be reconstructed with current approaches that do strongly depend on a high degree of cardiac motion periodicity for working properly. In a last year’s MICCAI contribution a first algorithm was presented that is able to estimate non-periodic 4-D motion patterns. However, to some degree that algorithm still depends on periodicity, as it requires a prior image which is obtained using a simple ECG-gated reconstruction. In this work we aim to provide a solution to this problem by developing a motion compensated ECG-gating algorithm. It is built upon a 4-D timecontinuous affine motion model which is capable of compactly describing highly non-periodic motion patterns. A stochastic optimization scheme is derived which minimizes the error between the measured projection data and the forward projection of the motion compensated reconstruction. For evaluation, the algorithm is applied to 5 datasets of the left coronary arteries of patients that have ignored the breath hold command and/or had arrhythmic heart signals during the data acquisition. By applying the developed algorithm the average visibility of the vessel segments could be increased by 27%. The results show that the proposed algorithm provides excellent reconstruction quality in cases where classical approaches fail. The algorithm is highly parallelizable and a clinically feasible runtime of under 4 minutes is achieved using modern graphics card hardware

SPEER - A new family of testis-specific genes from the mouse

© 2003 by the Society for the Study of ReproductionAndrej-Nikolai Spiess, Norbert Walther, Nadine Muller, Marga Balvers, Christoph Hansis, and Richard Ivel