This brief review article discusses marital dissolution and health with a focus on two specific themes. First, we introduce and discuss the search for plausible causal pathways that link the end of marriage to distal health outcomes. Second, we suggest that the socioeconomic status disruptions that follow divorce represent a plausible causal pathway and emphasize the need for more psychological science in this area of study. Although there is substantial literature that demonstrates that divorced adults, especially divorced women, experience significant financial disruptions, the research in this area remains broad and largely the province of family sociology and demography. Research is needed to better understand adults' psychological and behavioral responses to changes in their financial situation after the end of marriage.How people choose to spend money is often observable to others (e.g. based on their clothes, accessories, and social media pages), but there is a whole universe of financial decisions that are essentially unobservable (e.g. how people handle their debts, taxes, and retirement planning). We explore one context where people have an up-close-and-personal view of someone else's financial decision-making process romantic relationships. We discuss how the endless opportunities for financial observation in romantic relationships influence a range of behaviors, including spending habits, decisions about bank account structure, and financial infidelity. Our review highlights the need for more research on the ways in which financial decisions are made, communicated, and observed within romantic relationships.Many citizens distrust powerful societal institutions, and hold conspiracy theories about them. What are the implications of this suspicion of institutions for people's social relationships? The current paper proposes that institutions have at least two functions to regulate citizens' social relationships providing people with a sense of safety, and providing models for group norms and values. Suspicion of institutions undermines both of these functions, and therefore yields a range of negative societal outcomes by impacting people's interpersonal, within-group, and between-group relationships. More specifically, suspicion of institutions reduces trust between strangers, within-group cooperation, commitment, and prosocial behavior, and increases prejudice, intergroup conflict, polarization, and extremism. We conclude that institutional distrust and conspiracy theories erode the fabric of society.
  Restenosis after vessel angioplastydue to dedifferentiation of the vascular smooth muscle cells (VSMCs) limits the success of surgical treatment of vascular occlusions. Type 2 diabetes (T2DM) has a major impact on restenosis, with patients exhibiting more aggressive forms of vascular disease and poorer outcomes after surgery.  https://www.selleckchem.com/products/td139.html  Kv1.3 channels are critical players in VSMC proliferation. Kv1.3 blockers inhibit VSMCs MEK/ERK signalling and prevent vessel restenosis. We hypothesize that dysregulation of microRNAs (miR) play critical roles in adverse remodelling, contributing to Kv1.3 blockers efficacy in T2DM VSMCs.
 
  We used clinically relevant in vivo models of vascular risk factors (VRF) and vessels and VSMCs from T2DM patients.
 
  Human T2DM vessels showed increased remodelling, and changes persisted in culture, with augmented VSMCs migration and proliferation. Moreover, there were downregulation of PI3K/AKT/mTOR and upregulation of MEK/ERK pathways, with increased miR-126 expression. The inhibitory effects of Kv1.3 blockers on remodelling were significantly enhanced in T2DM VSMCs and in VRF model. Finally, miR-126 overexpression confered "diabetic" phenotype to non-T2DM VSMCs by downregulating PI3K/AKT axis.
 
  miR-126 plays crucial roles in T2DM VSMC metabolic memory through activation of MEK/ERK pathway, enhancing the efficacy of Kv1.3 blockers in the prevention of restenosis in T2DM patients.
 miR-126 plays crucial roles in T2DM VSMC metabolic memory through activation of MEK/ERK pathway, enhancing the efficacy of Kv1.3 blockers in the prevention of restenosis in T2DM patients.
  The current study addresses the cellular complexity and plasticity of subcutaneous (inguinal) white adipose tissue (iWAT) in mice during the critical periods of perinatal growth and establishment.
 
  We performed a large-scale single cell transcriptomic (scRNA-seq) and epigenomic (snATAC-seq) characterization of cellular subtypes (adipose stromal cells (ASC) and adipocyte nuclei) during inguinal WAT (subcutaneous; iWAT) development in mice, capturing the early postnatal period (postnatal days (PND) 06 and 18) through adulthood (PND56).
 
  Perinatal and adult iWAT contain 3 major ASC subtypes that can be independently identified by RNA expression profiles and DNA transposase accessibility. Furthermore, the transcriptomes and enhancer landscapes of both ASC and adipocytes dynamically change during postnatal development. Perinatal ASC (PND06) are highly enriched for several imprinted genes (IGs; e.g., Mest, H19, Igf2) and extracellular matrix proteins whose expression then declines prior to weaning (PND18). By clution, with important implications for the field of metabolic programming.
  Metabolic dysfunction can cause IL-1β mediated activation of the innate immune system, which could have important implications for the therapeutic efficacy of IL-1β neutralizing drugs as treatment for OA in the context of metabolic syndrome (MetS). In the present study, we investigated whether early treatment with a single dose of IL-1β blocking antibodies could prevent Western diet (WD) induced changes to systemic monocyte populations and their cytokine secretion profile and herewith modulate collagenase induced osteoarthritis (CiOA) pathology.
 
  CiOA was induced in female C57Bl/6 mice fed either a standard diet (SD) or WD and treated with a single dose of either polyclonal anti-IL-1β antibodies or control. Monocyte subsets and granulocytes in bone marrow and blood were analyzed with flow cytometry, and cytokine expression by bone marrow cells was analyzed using qPCR. Synovial cellularity, cartilage damage and osteophyte formation were assessed on histology.
 
  WD feeding of C57Bl/6 mice led to increased serum levels of low-density lipoprotein (LDL) and innate immune activation in the form of an increased number of Ly6C
  cells in bone marrow and blood and increased cytokine expression of IL-6 and TNF-α by bone marrow cells.