Exploring single-shot propagation and speckle based phase recovery techniques for object thickness estimation by using a polychromatic X-ray laboratory source.

Purpose: Propagation and speckle-based techniques allow reconstruction of the phase of an X-ray beam with a simple experimental setup. Furthermore, their implementation is feasible using low-coherence laboratory X-ray sources. We investigate different approaches to include X-ray polychromaticity for sample thickness recovery using such techniques. Approach: Single-shot Paganin (PT) and Arhatari (AT) propagation-based and speckle-based (ST) techniques are considered. The radiation beam polychromaticity is addressed using three different averaging approaches. The emission-detection process is considered for modulating the X-ray beam spectrum. Reconstructed thickness of three nylon-6 fibers with diameters in the millimeter-range, placed at various object-detector distances are analyzed. In addition, the thickness of an in-house made breast phantom is recovered by using multi-material Paganin's technique (MPT) and compared with micro-CT data. Results: The best quantitative result is obtained for the PT and ST combined with sample thickness averaging (TA) approach that involves individual thickness recovery for each X-ray spectral component and the smallest considered object-detector distance. The error in the recovered fiber diameters for both techniques is < 4 % , despite the higher noise level in ST images. All cases provide estimates of fiber diameter ratios with an error of 3% with respect to the nominal diameter ratios. The breast phantom thickness difference between MPT-TA and micro-CT is about 10%. Conclusions: We demonstrate the single-shot PT-TA and ST-TA techniques feasibility for thickness recovery of millimeter-sized samples using polychromatic microfocus X-ray sources. The application of MPT-TA for thicker and multi-material samples is promising.

The lack of EphB3 receptor prevents bone loss in mouse models of osteoporosis.

Bone homeostasis is a complex process in which some Eph kinase receptors and their ephrin ligands appear to be involved. In the present study, we address this issue by examining, both in vitro and in vivo, the role of EphB2 and EphB3 in mesenchymal stromal/stem cell (MSC) differentiation into bone tissue. This was first evaluated by quantitative reverse transcription PCR (RT-qPCR) and histological staining in MSCs cultured in specific mediums revealing that although EphB2-/- MSCs mainly expressed pro-adipogenic transcription factors, EphB3-/- MSCs showed abundant osteogenic transcripts, such as Runx2, Msx2, and Sp7. To clarify the underlying molecular mechanisms, we found that the lack of EphB3 signaling alters the genetic profile of differentiating MSCs, reducing the expression of many inhibitory molecules and antagonists of the BMP signaling pathway, and increasing Bmp7 expression, a robust bone inductor. Then, to confirm the osteogenic role of EphB3 in vivo, we studied the condition of 2 mouse models of induced bone loss (ovariectomy or long-term glucocorticoid treatment). Interestingly, in both models, both WT and EphB2-/- mice equally developed the disease but EphB3-/- mice did not exhibit the typical bone loss, nor an increase in urine Ca2+ or blood serum CTX-1. This phenotype in EphB3-KO mice could be due to their significantly higher proportions of osteoprogenitor cells and preosteoblasts, and their lower number of osteoclasts, as compared with WT and EphB2-KO mice. Thus, we conclude that EphB3 acts as a negative regulator of the osteogenic differentiation, and its absence prevents bone loss in mice subjected to ovariectomy or dexamethasone treatment.

Osteoporosis affects more than 200 million people, mostly women. Our work shows that the EphB3 receptor restricts bone formation, and its absence prevents bone loss in osteoporotic mice. The bone protection observed in EphB3-deficient mice is due to the presence of more bone-forming cells and fewer bone-degrading cells. Molecularly, we found that when there's no EphB3 in mesenchymal stem cells, some bone-promoting genes are increased while many inhibitors are reduced. Therefore, this receptor could become a key target for new therapies that would help to improve the quality of life for those suffering from bone diseases. We're really excited to share our findings with a broad audience, including patients, healthcare professionals, researchers, and the life sciences industry.

Resistance to Degradation of Silk Fibroin Hydrogels Exposed to Neuroinflammatory Environments.

Central nervous system (CNS) diseases represent an extreme burden with significant social and economic costs. A common link in most brain pathologies is the appearance of inflammatory components that can jeopardize the stability of the implanted biomaterials and the effectiveness of therapies. Different silk fibroin scaffolds have been used in applications related to CNS disorders. Although some studies have analyzed the degradability of silk fibroin in non-cerebral tissues (almost exclusively upon non-inflammatory conditions), the stability of silk hydrogel scaffolds in the inflammatory nervous system has not been studied in depth. In this study, the stability of silk fibroin hydrogels exposed to different neuroinflammatory contexts has been explored using an in vitro microglial cell culture and two in vivo pathological models of cerebral stroke and Alzheimer's disease. This biomaterial was relatively stable and did not show signs of extensive degradation across time after implantation and during two weeks of in vivo analysis. This finding contrasted with the rapid degradation observed under the same in vivo conditions for other natural materials such as collagen. Our results support the suitability of silk fibroin hydrogels for intracerebral applications and highlight the potentiality of this vehicle for the release of molecules and cells for acute and chronic treatments in cerebral pathologies.