This practice-led research article traces the development of Entangled Vessels, a series of plasma-illuminated borosilicate glass sculptures whose forms, materials and processes are entangled with circulatory metaphors drawn from both biology and physics. Working at the intersection of glass-blowing, neon fabrication and scientific glass-working, the author draws on the dual etymology of plasma, as both an ionised state of matter made luminous and a vascular component of blood, to investigate plasma illumination as a responsive and relational medium. The article explores how the experience of blood plasma donation during the COVID-19 pandemic, encounters with historical representations of circulatory systems, and technical mentorships with neon practitioners, scientific glassmakers and international plasma illumination practitioners converged to shape an experimental art practice. Central to this inquiry is the manifold: the apparatus through which glass vessels undergo atmospheric manipulation. Positioned not as a neutral tool but as an active participant in the making process, the manifold becomes a conceptual and material site of connectivity, containment and circulation. Through capacitive illumination, in which plasma vessels glow symbiotically within electromagnetic fields, brightening in response to a viewer's proximity and touch, these works make visible the typically invisible relationships between bodies, objects and energy. The article argues that plasma illumination, considered through Karen Barad's term intra-action, offers a medium uniquely capable of revealing our imperceptible interconnectedness.

Potassium homeostasis is maintained primarily by the kidney, yet potassium is increasingly recognized not only as a regulated electrolyte but also as a key determinant of renal physiology and kidney health. Experimental, epidemiologic, and clinical evidence supports a reciprocal relationship in which kidney function governs potassium balance, whereas dietary potassium intake and plasma potassium concentration influence renal sodium transport, blood pressure regulation, and susceptibility to kidney injury. Both potassium deficiency and excess are associated with adverse cardiorenal outcomes, emphasizing the importance of maintaining potassium within an optimal physiologic range. Evidence suggests that the kidney adapts to changes in potassium availability through coordinated feedforward and feedback mechanisms, including a putative gut-kidney signaling axis and nephron-intrinsic potassium-sensing pathways. Along the nephron, inwardly rectifying potassium channels function as extracellular potassium sensors that couple changes in potassium concentration to alterations in epithelial transport and metabolism. Recent studies have identified potassium-responsive signaling pathways in the proximal tubule that regulate sodium transport, cellular growth, and kidney injury during potassium deficiency. In the distal convoluted tubule, related mechanisms regulate the thiazide-sensitive sodium-chloride cotransporter through the renal "potassium switch," linking potassium balance to sodium handling and blood pressure control. These mechanistic advances have renewed interest in potassium supplementation and potassium-containing additives as therapeutic interventions. Epidemiologic and emerging clinical data suggest that physiologically appropriate potassium intake, particularly from potassium-rich diets or bicarbonate/citrate-containing supplements, may provide cardiovascular and renal benefits. However, because impaired potassium excretion increases susceptibility to hyperkalemia in advanced chronic kidney disease, potassium supplementation and restriction should be individualized according to kidney function and patient risk.

Synonymous recoding is widely used to enhance therapeutic protein expression, yet its broader effects on biogenesis and function remain unclear. We systematically examined how synonymous recoding shapes protein structure, processing, and activity using plasma protease ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 repeats, member 13) and its truncated MDTCS (metalloprotease, disintegrin-like, thrombospondin type 1, cysteine-rich, and spacer) variant across cell-free expression, transient transfection, lentiviral delivery, and targeted genomic integration. Wild-type, codon-optimized, and codon-pair-optimized constructs displayed pronounced, system-dependent differences in intracellular proteolysis, secretion, enzymatic performance, and post-translational modifications. Targeted genomic integration produced the highest protein fidelity, whereas transient and lentiviral systems yielded lower extracellular protein levels, particularly for codon-pair-optimized variants. Glycoproteomic analyses revealed distinct glycosylation patterns among synonymous constructs, indicating altered maturation, while Ankyron-based assays detected differences in molecular surface properties of recoding variants. Optimized MDTCS exhibited increased catalytic activity but reduced substrate affinity. These findings demonstrate that synonymous recoding can reshape proteostasis and activity, emphasizing the need for comprehensive evaluation of engineered therapeutic genes beyond yield.

Advancements in the management of muscle-invasive bladder cancer have increasingly focused on strategies that balance oncologic control with preservation of quality of life. The therapeutic landscape for neoadjuvant therapy is rapidly evolving as immunotherapy and novel agents are integrated into systemic therapy regimens. The utility of tumor tissue, plasma, and urine biomarkers in selecting patients for bladder preservation remains uncertain and warrants further evaluation in prospective clinical trials before incorporation into routine clinical practice. Clinicians should consider both tumor-specific factors and patient-specific factors when engaging in shared decision-making.

Schizophrenia (SCZ) and systemic lupus erythematosus (SLE) exhibit epidemiological overlap, suggesting shared genetic underpinnings. Using the largest SLE genome-wide association study (GWAS) to date, we identified a significant genetic correlation between SCZ and SLE (rg = 0.25, p = 9.0 × 10-4). Cross-trait analysis nominated multiple candidate shared loci outside the major histocompatibility complex (MHC), most with aligned effects. The strongest candidate shared association was found at the FURIN-FES locus, previously implicated in SCZ and newly associated with SLE. In addition to FURIN-FES, FCGR2A, DOT1L and an intergenic noncoding RNA locus on chromosome 2 showed additional evidence consistent with shared association. Functional annotation showed that this locus modulated the expression of FURIN, which encodes a proprotein convertase involved in diverse biological processes, and FES, which encodes a tyrosine kinase important in innate immune signalling. The shared risk allele was also associated with altered plasma levels of FURIN, FES, and their functional partners (GDF2, BMP10, NTF4, FER). Tissue- and cell-type-specific eQTL analysis revealed distinct regulatory effects: FURIN expression was perturbed in neuronal and immune cells, while FES expression was altered in immune cells. Mendelian randomisation supported a causal role for FES protein in both disorders. These findings highlight that pleiotropy at the FURIN-FES locus for SCZ and SLE is compatible with disease-specific mechanisms. This underscores that shared genetics across traits does not necessarily mean shared biology.

The health effects of moderate consumption of pasture-raised red meat within healthy dietary patterns remain uncertain.

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive fibrotic lung disease with an extremely poor prognosis, and the rate of disease progression varies significantly among patients. Therefore, accurate prognostic assessment is crucial for clinical management. Traditional pulmonary function parameters, such as the absolute value of forced vital capacity (FVC) and the rate of decline in FVC as a percentage of predicted value (FVC%), serve as important bases for predicting disease progression and mortality. In recent years, prognostic prediction models have evolved from single indicators to composite scoring systems that integrate physiological, imaging, clinical manifestations, and even biomarkers. Furthermore, emerging indicators such as quantitative assessment of fibrosis extent on high-resolution computed tomography (HRCT), serum biomarkers, and artificial intelligence-based radiomics analysis provide powerful tools for earlier and more accurate identification of patients at risk of rapid disease progression. However, how to effectively incorporate these emerging indicators into clinical practice and clinical trials remains a current challenge. Future research should focus on validating and optimizing multi-omics prediction models, exploring their application value in individualized risk stratification and guiding treatment decisions for patients, with the ultimate goal of improving the long-term prognosis of IPF patients.

Per- and polyfluoroalkyl substances (PFAS) represent a formidable class of persistent synthetic chemicals whose contamination of the global food supply, particularly through animal products, constitutes a major and direct route of human exposure. This review synthesizes the current scientific understanding of PFAS entry into food animal production systems including livestock, poultry, and aquaculture via contaminated feed, water, and soil. We detail the subsequent toxicokinetics in animals, which lead to pronounced tissue-specific bioaccumulation. Two distinct and non-interchangeable rankings are therefore applied throughout this review. On a concentration basis (ng g-1 wet weight in the edible matrix), liver and kidney consistently exceed muscle by approximately one to two orders of magnitude within the same animal, while among marketed commodities the descending order is generally offal > certain seafood > eggs > milk and dairy ≈ muscle meat. On a population dietary-intake basis (ng kg-1 body weight week-1), the ranking reverses for several commodities because intake is the product of concentration and consumption: seafood, muscle meat, eggs and dairy dominate total intake in most national diets, whereas offal contributes episodic high-dose exposure in a minority of consumers. The analysis confirms that animal-derived foods are a dominant contributor to dietary PFAS intake. Epidemiological studies report consistent positive associations between the consumption of these commodities and human serum concentrations; such associations characterize internal exposure and source attribution, and are distinguished here from formal risk characterization, which requires comparison of estimated intakes with health-based guidance values such as the EFSA tolerable weekly intake of 4.4 ng kg-1 body weight week-1 for the sum of PFOA, PFNA, PFHxS and PFOS. We critically examine the fragmented and lagging regulatory landscape governing PFAS in food, highlighting significant data gaps concerning novel replacement compounds and mixture effects. The review concludes that mitigating this public health threat requires an integrated "Farm-to-Fork" strategy, encompassing source control in agriculture, proactive food safety monitoring, and the development of harmonized international standards. Addressing PFAS contamination in food animals is therefore not merely an environmental issue but an urgent imperative for safeguarding food security and public health.

Autoantibodies to insulinoma-associated antigen 2 (IA2) are well-established biomarkers of islet autoimmunity, supporting the diagnosis and risk stratification of type 1 diabetes (T1D). This study presents the analytical and clinical evaluation of a newly developed bridge-type Anti-IA2 ELISA (Euroimmun), which is CE-marked under the European In Vitro Diagnostic Regulation (IVDR) and compatible with fully automated processing platforms. The analytical performance was assessed through precision, detection capability, linearity, and interference studies. Diagnostic accuracy testing and method comparison with the predecessor ELISA and the Medipan CentAK anti-IA2 M radioimmunoassay were performed using serum samples from patients with T1D (median age at diagnosis: 11 years; median diabetes duration: 4 years), latent autoimmune diabetes in adults, or Addison's disease, as well as samples from non-T1D control groups and the Islet Autoantibody Standardization Program (IASP). The assay demonstrated low intra-/inter-lot imprecision (CVs ≤ 3.2%), detection limits in the low IU/mL range, linearity over the measuring range (10-2000 IU/mL), and no interference from hemolytic, lipemic, or icteric sample conditions. Sensitivity was 53.8% in the clinical T1D cohort (56.5% in newly diagnosed patients), and 76.0% in IASP case samples. Specificity in non-T1D controls reached 98.4%. Agreement with the predecessor ELISA was almost perfect (94.7%; κ = 0.873). Compared with the radioimmunoassay, substantial agreement (82.4-83.8%; κ ≥ 0.637) was observed, and the ELISA identified more anti-IA2-positive T1D samples. In conclusion, the new Anti-IA2 ELISA combines strong analytical and diagnostic performance with a fully automated workflow enabling standardized end-to-end processing. These features support implementation in high-throughput routine diagnostics. Prospective validation in larger and population-representative cohorts is warranted to further assess the assay's suitability for potential future use in large-scale screening aimed at improving early detection and risk assessment in autoimmune diabetes.