Background: A vast body of research has demonstrated that disease susceptibility and offspring health can be influenced by perinatal factors, which include both paternal and maternal behavior and environment. Offspring disease risk has the potential to affect the health span and life span of offspring. Key Findings: Various maternal factors, such as environmental toxicant exposure, diet, stress, exercise, age at conception, and longevity have the potential to influence age-associated diseases such as cardiovascular disease, obesity, diabetes, and cancer risk in offspring. Paternal factors such as diet, age at conception, and longevity can potentially impact offspring health span and life span-reducing traits as well. Practical Implications: Continued research could go a long way toward defining mechanisms of the developmental origins of life span and health span, and eventually establishing regimens to avoid negative developmental influences and to encourage positive interventions to potentially increase life span and improve health span in offspring.

Low circulating taurine concentrations have been proposed as a driver of the aging process. We found that circulating taurine concentrations increased or remained unchanged with age in three geographically distinct human cohorts as well as in nonhuman primates and mice when measured longitudinally (repeatedly in the same population) or cross-sectionally (sampling distinct populations at various ages). Moreover, considerable variability was observed in associations between taurine and age-related changes in health outcomes pertaining to gross motor function and energy homeostasis. Our results suggest that changes in circulating taurine are not a universal feature of aging and that its pleiotropic effects may be dependent on the temporal and physiological context of each individual.

New Findings: What is the central question of this study? Is chemerin, an adipokine implicated in obesity, increased in neonates following in utero cigarette smoke exposure. What is the main finding and its importance? Chemerin mRNA expression was increased and chemerin DNA methylation was decreased in babies born to mothers who smoked during pregnancy. These data provide a potential mechanism that may be mediating the increased obesity risk in individuals that are born to mothers who smoked during pregnancy. It has been shown that in utero tobacco exposure increases offspring risk for obesity, but the mechanisms responsible for this increased risk are not well understood. Chemerin is an adipokine that regulates adipocyte differentiation. This chemokine is elevated in obese individuals and with smoke exposure, but its levels have not been measured in neonates exposed to cigarette smoke in utero. We examined chemerin gene expression [n = 31 non‐smoker (NS) and 15 smoker (S)] and DNA methylation (n = 28 NS and n = 11 S) in skin collected from babies born to mothers who smoked during pregnancy as compared to non‐smoking controls. Quality RNA and DNA were isolated from foreskin tissue following circumcision, and chemerin gene expression and DNA methylation were assessed. Further, in a second cohort, we utilized primary dermal foreskin fibroblasts as a functional measure of adipogenesis in living cells (n = 11 NS and n = 8 S). Cells were stimulated with an adipogenic cocktail, mRNA was isolated from cells after 14 days, and chemerin gene expression assessed via real‐time PCR. Chemerin mRNA was elevated in both whole tissue (NS: 2409.20 ± 555.28 counts and S: 2966.72 ± 636.84 counts; P < 0.01) and primary fibroblasts (NS: 1.12 ± and S: 2.13 ± ; P = 0.04) collected from infants born to smoking mothers. Chemerin DNA methylation was reduced in whole tissue of offspring born to smokers (NS: 4.18 ± 1.28 and S: 3.07 ± 1.31%; P = 0.02), which may contribute to the increased gene expression. Neonates born to mothers who smoke during pregnancy exhibit distinct changes in chemerin gene expression in response to in utero tobacco smoke exposure which are regulated in part by epigenetic alterations.

Cutaneous T-cell lymphoma (CTCL) is a rare hematologic malignancy that traditionally presents with cutaneous lesions, though metastases are not uncommon in progressive disease. We describe four cas... Plain language summary Cutaneous T-cell lymphoma (CTCL) is a rare cancer of the blood, which typically manifests with skin lesions, such as itchy, scaly rashes that may thicken to form tumors on th... Graphical abstract

Clinical research dissemination is frequently hindered by administrative friction and methodological inconsistency. To address these barriers, we developed TernTables, a freely available, open-source web application (https://www.tern-tables.com/) and R package (https://cran.r-project.org/package=TernTables) that streamlines the transition from raw data to formatted results for descriptive and univariate clinical reporting. The system integrates a client-side screening protocol for protected health information (PHI) with a rule-based decision tree that selects and executes appropriate frequency-based, parametric, or non-parametric statistical tests based on data distribution and class. TernTables generates publication-ready summary tables in Microsoft Word format, complemented by dynamically generated methods text and the underlying R code to ensure complete transparency and reproducibility. Validation using a landmark clinical trial dataset demonstrated concordance with established biostatistical approaches for descriptive and univariate analyses. TernTables is designed to supplement, not replace, formal statistical consultation by standardizing routine descriptive and univariate workflows, allowing biostatistical expertise to be focused on complex analyses and study design. By lowering technical and financial barriers, the platform democratizes access to rigorous statistical workflows while maintaining methodological excellence and reducing "researcher degrees of freedom."