Core-periphery structure, the arrangement of a network into a dense core and sparse periphery, is a versatile descriptor of various social, biological, and technological networks. In practice, different core-periphery algorithms are often applied interchangeably despite the fact that they can yield inconsistent descriptions of core-periphery structure. For example, two of the most widely used algorithms, the k-cores decomposition and the classic two-block model of Borgatti and Everett, extract fundamentally different structures The latter partitions a network into a binary hub-and-spoke layout, while the former divides it into a layered hierarchy. We introduce a core-periphery typology to clarify these differences, along with Bayesian stochastic block modeling techniques to classify networks in accordance with this typology. Empirically, we find a rich diversity of core-periphery structure among networks.  https://www.selleckchem.com/products/BIBF1120.html  Through a detailed case study, we demonstrate the importance of acknowledging this diversity and situating networks within the core-periphery typology when conducting domain-specific analyses.Adult neurogenesis in the dentate gyrus of the hippocampus is regulated by specific microglia groups and functionally implicated in behavioral responses to stress. However, the role of microglia in hippocampal neurogenesis and stress resilience remains unclear. We identified interleukin 4 (IL4)-driven microglia characterized by high expression of Arg1, which is critical in maintaining hippocampal neurogenesis and stress resistance. Decreasing Arg1+ microglia in the hippocampus by knocking down the microglial IL4R suppressed hippocampal neurogenesis and enhanced stress vulnerability. Increasing Arg1+ microglia in the hippocampus by enhancing IL4 signaling restored hippocampal neurogenesis and the resilience to stress-induced depression. Brain-derived neurotrophic factor (BDNF) was found necessary for the proneurogenesis effects of IL4-driven microglia. Together, our findings suggest that IL4-driven microglia in the hippocampus trigger BDNF-dependent neurogenesis responding to chronic stress, helping protect against depressive-like symptoms. These findings identify the modulation of a specific microglial phenotype as a treatment strategy for mood disorders.Turbulence, the ubiquitous and chaotic state of fluid motions, is characterized by strong and statistically nontrivial fluctuations of the velocity field, and it can be quantitatively described only in terms of statistical averages. Strong nonstationarities impede statistical convergence, precluding quantifying turbulence, for example, in terms of turbulence intensity or Reynolds number. Here, we show that by using deep neural networks, we can accurately estimate the Reynolds number within 15% accuracy, from a statistical sample as small as two large-scale eddy turnover times. In contrast, physics-based statistical estimators are limited by the convergence rate of the central limit theorem and provide, for the same statistical sample, at least a hundredfold larger error. Our findings open up previously unexplored perspectives and the possibility to quantitatively define and, therefore, study highly nonstationary turbulent flows as ordinarily found in nature and in industrial processes.Placed in a historic context, this overview focuses on post-transpant pregnancy, fatherhood, and contraception in women and men. The critical importance of early reproductive counseling because of improved sexual function and the early return of ovulation and menses post-transplant is emphasized. We explain the decision making regarding contraception choices. The available data on the safety of immunosuppressive drugs in pregnancy, and for men desiring fatherhood, are detailed. The risk of maternal ingestion of mycophenolate products on the in utero fetus is considered and contrasted with the lack of concern for their use by men fathering children. Pregnancy risks to the allograft, baby, and mother are discussed. An infant's exposure to specific immunosuppressant medications through breastfeeding is reviewed. The ethics and realities of post-transplant parenthood are explored.Caseinolytic mitochondrial matrix peptidase proteolytic subunit (CLPP) is a serine protease that degrades damaged or misfolded mitochondrial proteins. CLPP-null mice exhibit growth retardation, deafness, and sterility, resembling human Perrault syndrome, but also display immune system alterations. However, the molecular mechanisms and signaling pathways underlying immunological changes in CLPP-null mice remain unclear. In this study, we report the steady-state activation of type I IFN signaling and antiviral gene expression in CLPP-deficient cells and tissues, resulting in marked resistance to RNA and DNA virus infection. Depletion of the cyclic GMP-AMP (cGAS)-stimulator of IFN genes (STING) DNA sensing pathway reduces steady-state IFN-I signaling and abrogates the broad antiviral phenotype of CLPP-null cells. Moreover, we report that CLPP deficiency leads to mitochondrial DNA (mtDNA) instability and packaging alterations. Pharmacological and genetic approaches to deplete mtDNA or inhibit cytosolic release markedly reduce antiviral gene expression, implicating mtDNA stress as the driver of IFN-I signaling in CLPP-null mice. Our work places the cGAS-STING-IFN-I innate immune pathway downstream of CLPP and may have implications for understanding Perrault syndrome and other human diseases involving CLPP dysregulation.The prime function of proteasomes is the control of protein homeostasis in cells (i.e., the removal of proteins that are not properly folded, damaged by stress conditions like reactive oxygen species formation, or degraded on the basis of regular protein turnover). During viral infection, the standard proteasome is replaced by the so-called immunoproteasome (IP) in an IFN-γ-dependent manner. It has been proposed that the IP is required to protect cell viability under conditions of IFN-induced oxidative stress. In this study, we investigated the requirement for IP to cope with the enhanced need for protein degradation during lymphocytic choriomeningitis virus (LCMV) infection in mice lacking the IP subunit LMP7. We found that IP are upregulated in the liver but not in the spleen during LCMV infection, although the total proteasome content was not altered. The expression of standard proteasome subunits is not induced in LMP7-deficient mice, indicating that enhanced proteasomal activity is not required during viral infection.