In posttraumatic stress disorder (PTSD), functional connectivity (FC) between the thalamus and other brain areas has yet to be comprehensively investigated. The present study explored resting state FC (rsFC) of thalamus and its associations with trauma-related features. The included subjects were North Korean refugees with PTSD (n = 23), trauma-exposed North Korean refugees without PTSD (trauma-exposed control [TEC] group, n = 22), and South Korean healthy controls (HCs) without traumatic experiences (HC group, n = 40). All participants underwent psychiatric evaluation and functional magnetic resonance imaging (fMRI) procedures using the bilateral thalamus as seeds. In the TEC group, the negative rsFC between each thalamus and its contralateral postcentral cortex was stronger relative to the PTSD and HC groups, while positive rsFC between the left thalamus and left precentral cortex was stronger in the HC group compared to the PTSD and TEC groups. Thalamo-postcentral rsFC was positively correlated with the CAPS total score in the TEC group, and with the number of traumatic experiences in the PTSD group. The present study identified the difference of thalamic rsFC alterations among traumatized refugees and HCs. Negative rsFC between the thalamus and somatosensory cortices might be compensatory changes after multiple traumatic events in refugees.The MEN1 gene, a tumor suppressor gene that encodes the protein menin, is mutated at high frequencies in neuroendocrine (NE) tumors; however, the biological importance of this gene in NE-type lung cancer in vivo remains unclear. Here, we established an ATII-specific KrasG12D/+/Men1-/- driven genetically engineered mouse model and show that deficiency of menin results in the accumulation of DNA damage and antagonizes oncogenic Kras-induced senescence and the epithelial-to-mesenchymal transition during lung tumorigenesis. The loss of menin expression in certain human primary lung cancers correlates with elevated NE profiles and reduced overall survival.Atherosclerosis is a multifactorial disease of the vasculature, and shear stress is a crucial regulator of its process. Disturbed flow promotes atherosclerotic effects, while laminar flow has a protective action on the endothelium.  https://www.selleckchem.com/products/cl-amidine.html  Hippo/YAP is a major cascade that senses various mechanical cues and mediates the expression of pro-inflammatory genes. However, the mechanism modulating the transcription factor YAP in response to different patterns of blood flow remains unclear. In this study, we provide evidence that shear stress modulates YAP activity via autophagy in endothelial cells. Laminar flow promoted the expression of the autophagic markers BECLIN 1 and LC3II/LC3I. Autophagy blockade using a chemical inhibitor repressed YAP degradation under laminar flow. Conversely, the induction of autophagy under disturbed flow partially antagonized the nuclear import and transcriptional activation of YAP. In parallel, laminar flow led to the increased expression of SIRT1 protein, a NAD+-dependent deacetylase. Further investigation showed that SIRT1-mediated YAP deacetylation. The forced expression of SIRT1 under disturbed flow effectively attenuated YAP activation and nuclear accumulation, thereby downregulating the expression of pro-inflammatory genes. In atheroprone vessels of mice receiving rapamycin to induce autophagy, the enhanced expression of SIRT1 was observed together with YAP repression. Altogether, these results show that endothelial autophagy and SIRT1 expression induced by laminar flow contribute to the inhibition of Hippo/YAP signaling and interrupt atherosclerotic plaque formation.The success of filamentous fungi in colonizing most natural environments can be largely attributed to their ability to form an expanding interconnected network, the mycelium, or thallus, constituted by a collection of hyphal apexes in motion producing hyphae and subject to branching and fusion. In this work, we characterize the hyphal network expansion and the structure of the fungus Podospora anserina under controlled culture conditions. To this end, temporal series of pictures of the network dynamics are produced, starting from germinating ascospores and ending when the network reaches a few centimeters width, with a typical image resolution of several micrometers. The completely automated image reconstruction steps allow an easy post-processing and a quantitative analysis of the dynamics. The main features of the evolution of the hyphal network, such as the total length L of the mycelium, the number of "nodes" (or crossing points) N and the number of apexes A, can then be precisely quantified. Beyond these main features, the determination of the distribution of the intra-thallus surfaces (Si) and the statistical analysis of some local measures of N, A and L give new insights on the dynamics of expanding fungal networks. Based on these results, we now aim at developing robust and versatile discrete/continuous mathematical models to further understand the key mechanisms driving the development of the fungus thallus.Low doses of ionizing radiation (LDIR) activate endothelial cells inducing angiogenesis. In zebrafish, LDIR induce vessel formation in the sub-intestinal vessels during post-embryonic development and enhance the inter-ray vessel density in adult fin regeneration. Since angiogenesis is a crucial process involved in both post-embryonic development and regeneration, herein we aimed to understand whether LDIR accelerate these physiological conditions. Our data show that LDIR upregulate the gene expression of several pro-angiogenic molecules, such as flt1, kdr, angpt2a, tgfb2, fgf2 and cyr61in sorted endothelial cells from zebrafish larvae and this effect was abrogated by using a vascular endothelial growth factor receptor (VEGFR)-2 tyrosine kinase inhibitor. Irradiated zebrafish present normal indicators of developmental progress but, importantly LDIR accelerate post-embryonic development in a VEGFR-2 dependent signaling. Furthermore, our data show that LDIR do not accelerate regeneration after caudal fin amputation and the gene expression of the early stages markers of regeneration are not modulated by LDIR. Even though regeneration is considered as a recapitulation of embryonic development and LDIR induce angiogenesis in both conditions, our findings show that LDIR accelerate post-embryonic development but not regeneration. This highlights the importance of the physiological context for a specific phenotype promoted by LDIR.