The increasing number of older people is resulting in an increased prevalence of age-related diseases. Research has shown that the ageing process itself is a potential point of intervention. Indeed, gene expression can be optimised for health in older ages through manipulation of transcription factor (TF) activity. This review is focused on the ever-growing number of TFs whose effects on ageing are evolutionarily conserved. These regulate a plethora of functions, including stress resistance, metabolism, and growth. They are engaged in complex interactions within and between different cell types, impacting the physiology of the entire organism. Since ageing is not programmed, the conservation of their effects on lifespan is most likely a reflection of the conservation of their functions in youth. Cell size is fundamental to cell physiology because it sets the scale of intracellular geometry, organelles, and biosynthetic processes. In animal cells, size homeostasis is controlled through two phenomenologically distinct mechanisms. First, size-dependent cell cycle progression ensures that smaller cells delay cell cycle progression to accumulate more biomass than larger cells prior to cell division. Second, size-dependent cell growth ensures that larger and smaller cells grow slower per unit mass than more optimally sized cells. This decade has seen dramatic progress in single-cell technologies establishing the diverse phenomena of cell size control in animal cells. Here, we review this recent progress and suggest pathways forward to determine the underlying molecular mechanisms. When cells progress to malignancy, they must overcome a final telomere-mediated proliferative lifespan barrier called replicative crisis. Crisis is characterized by extensive telomere fusion that drives widespread genomic instability, mitotic arrest, hyperactivation of autophagy, and cell death. Recently, it has become apparent that that the resolution of dicentric chromosomes, which arise from telomere fusions during crisis, can initiate a sequence of events that leads to chromothripsis, a form of extreme genomic catastrophe. Chromothripsis is characterized by localized genomic regions containing tens to thousands of rearrangements and it is becoming increasingly apparent that chromothripsis occurs widely across tumor types and has a clinical impact. Here we discuss how telomere dysfunction can initiate genomic complexity and the emerging mechanisms of chromothripsis.  https://www.selleckchem.com/products/sodium-l-lactate.html  During scientific investigations, the explanation of remarkably interesting phenomena must often await development of new methods or accrual of new observations that in retrospect can lead to lucid answers to the initial problem. A case in point is the control of genetic recombination during meiosis, which leads to crossovers between chromosomes critical for production of healthy offspring. Crossovers must be properly placed along meiotic chromosomes for their accurate segregation. Here, we review observations on two aspects of meiotic crossover control - crossover interference and repression of crossovers near centromeres, both observed more than 85 years ago. Only recently have relatively simple molecular mechanisms for these phenomena become clear through advances in both methods and understanding the molecular basis of meiotic recombination. Quantitative trait loci (QTL) analysis is an important approach to investigate the effects of genetic variants identified through an increasing number of large-scale, multidimensional 'omics data sets. In this 'big data' era, the research community has identified a significant number of molecular QTLs (molQTLs) and increased our understanding of their effects. Herein, we review multiple categories of molQTLs, including those associated with transcriptome, post-transcriptional regulation, epigenetics, proteomics, metabolomics, and the microbiome. We summarize approaches to identify molQTLs and to infer their causal effects. We further discuss the integrative analysis of molQTLs through a multi-omics perspective. Our review highlights future opportunities to better understand the functional significance of genetic variants and to utilize the discovery of molQTLs in precision medicine. The only curative therapy for diseases such as organ failure is orthotopic organ transplantation. Organ transplantation has been limited due to the shortage of donor organs. The huge disparity between those who need and those who receive transplantation therapy drives the pursuit of alternative treatments. Therefore, novel therapies are warranted. Recent studies support the feasibility of generating human-porcine chimeras that one day would provide humanized vasculature and blood for transplantation and serve as important research models. The ethical issues they raise require open discussion and dialog lest promising lines of inquiry flounder due to unfounded fears or compromised public trust. In the event that human embryo genome editing is considered safe enough for the clinic, researchers will need to consider how to administer consent so that would-be recipients of edited embryos can make an informed decision. Informed consent will require truthfulness, sensitivity, regulatory compliance, and attention to the highest ethical standards. The omentum is a visceral adipose tissue rich in fat-associated lymphoid clusters (FALCs) that collects peritoneal contaminants and provides a first layer of immunological defense within the abdomen. Here, we investigated the mechanisms that mediate the capture of peritoneal contaminants during peritonitis. Single-cell RNA sequencing and spatial analysis of omental stromal cells revealed that the surface of FALCs were covered by CXCL1+ mesothelial cells, which we termed FALC cover cells. Blockade of CXCL1 inhibited the recruitment and aggregation of neutrophils at FALCs during zymosan-induced peritonitis. Inhibition of protein arginine deiminase 4, an enzyme important for the release of neutrophil extracellular traps, abolished neutrophil aggregation and the capture of peritoneal contaminants by omental FALCs. Analysis of omental samples from patients with acute appendicitis confirmed neutrophil recruitment and bacterial capture at FALCs. Thus, specialized omental mesothelial cells coordinate the recruitment and aggregation of neutrophils to capture peritoneal contaminants.