Colchicine is a widely utilised drug for the management of conditions such as gout, pericarditis and familial Mediterranean fever. It has a narrow therapeutic index, with a significant risk of toxicity in overdose leading to life-threatening consequences. We present a case of severe colchicine toxicity following ingestion of 20 mg (0.26 mg/kg), resulting in multi-organ failure requiring intensive care management. Rapid deterioration with hyperthermia, electrolyte derangement, rhabdomyolysis, coagulopathy and significant bone marrow suppression necessitated IV antibiotics, platelet transfusion and granulocyte colony-stimulating factor (GCSF) and subsequent admission to critical care for vasopressors and ventilatory support. The patient eventually improved with resolution of haematological and renal parameters, was reviewed by the mental health team and discharged with full functional recovery. This case underscores the importance of early recognition, aggressive supportive care, and multidisciplinary management of patients presenting with colchicine overdose, in order to achieve a favourable outcome. The unpredictable relationship between colchicine dose and clinical outcome highlights the need for close monitoring even following relatively low-dose ingestion. Increased clinician awareness of colchicine toxicity and its delayed manifestations is essential for timely intervention in such critical cases.

Point-of-care testing (POCT) demands rapid, user-friendly solutions for instant medical diagnosis. Traditional colorimetric whole-blood analysis faces challenges from red blood cell and hemoglobin interference, often necessitating complex pretreatment. Herein, we introduce a three-dimensional (3D) nanoporous hydrogel-integrated portable platform designed for pretreatment-free, rapid multiplexed detection of small-molecule biomarkers directly from whole blood. The platform utilizes a polystyrene Eppendorf (EP)-tube as a miniaturized laboratory, featuring a TiO2-sodium alginate hydrogel-modified cap with a 3D nanoscale porous architecture. This innovative structure serves dual roles: embedding enzymatic systems for cascade reactions and excluding macromolecules (e.g., hemoglobin, erythrocytes) through size-selective exclusion. Small-molecule biomarkers (e.g., glucose, uric acid, lactate) diffuse into the hydrogel matrix, triggering concentration-proportional colorimetric signals via enzymatic cascade reactions. A 15-min "flip-and-scan" protocol-comprising tube inversion for biomarker diffusion and smartphone RGB analysis for quantitative readout-enables simultaneous quantification of three biomarkers with detection limits of 0.11 mM for glucose, 16 μM for uric acid, and 20 μM for lactate. The clinical validation with diverse patient samples (diabetic, gout, and composite metabolic cases) demonstrates that the tri-marker detection strategy enables precise differential diagnosis of overlapping metabolic syndromes by distinguishing biomarker patterns. Clinical validation with 15 diverse patient samples (5 diabetic patients, 5 gout patients, and 5 patients with composite metabolic abnormalities) demonstrated strong concordance with a commercial clinical biochemistry analyzer, with Pearson correlation coefficient > 0.95 and negligible bias in Bland-Altman analysis with all data points falling within the 95% limits of agreement. Compared with conventional microfluidic and paper-based sensors, this approach eliminates pretreatment steps, reduces assay time, ensures closed-loop biosafety, and prevents cross-contamination, offering a versatile and accessible analytical platform that represents a significant step toward practical multiplexed biomarker detection in POCT.

Gout has become a rapidly expanding metabolic-inflammatory disease in China, but the long-term trajectory, changing attributable risks, and future burden among middle-aged adults remain incompletely defined. We assessed gout burden among Chinese adults aged 40 to 59 years from 1990 to 2023 and projected trends to 2035. Using Global Burden of Disease Study 2023 (GBD 2023) data, we analyzed gout prevalence, incidence, and disability-adjusted life years among Chinese adults aged 40 to 59 years. Joinpoint regression identified temporal inflection points; Das Gupta decomposition quantified contributions from population growth, aging, and epidemiological change; Bayesian age-period-cohort modeling projected burden to 2035; and population attributable fractions (PAFs) were estimated for high body mass index (BMI) and kidney dysfunction, with sex- and age-stratified analyses. Prevalent cases increased from 2.56 million in 1990 to 6.75 million in 2023, while the age-standardized prevalence rate rose by 21.08% (1226.32-1484.81 per 1,00,000). The steepest acceleration occurred during 2009 to 2018. Population growth accounted for approximately 70% to 73% of the absolute increase, epidemiological change for 19% to 24%, and aging for 6% to 8%. High BMI remained the dominant attributable risk factor, accounting for 32.2% of gout-related disability-adjusted life years in 2023, whereas the PAF attributable to kidney dysfunction declined from 6.5% to 4.7%. Men had a higher BMI-attributable PAF at ages 40 to 44 years, but women had a greater proportional burden from age 45 onward. Projections indicated that gout burden would remain at a high level through 2035. Gout burden among middle-aged adults in China has risen substantially and is increasingly shaped by metabolic risk. Population-level weight and dietary interventions, sex-sensitive prevention and screening, and guideline-concordant urate-lowering management are needed to curb the projected burden. As an ecological analysis of modeled estimates, these findings identify population-level associations rather than establish causation.

Ruzinurad ([®]) is an orally administered, small-molecule, selective inhibitor of urate transporter 1 (URAT1) that is being developed by the Jiangsu Hengrui Pharmaceuticals Co. for the treatment of hyperuricaemia associated with gout. By inhibiting the transport function of URAT1, ruzinurad suppresses uric acid reabsorption, thereby promoting uric acid excretion, leading to a reduction in serum uric acid levels. In May 2026, the National Medical Products Administration in China approved ruzinurad tablets for patients with hyperuricaemia associated with gout. This article summarises the milestones in the development of ruzinurad leading to this first approval for patients with hyperuricaemia associated with gout.

Cardiovascular disease represents the foremost cause of mortality globally. Annually, there are approximately 720,000 new cases of myocardial infarction and 335,000 recurrent events. Coronary artery bypass grafting (CABG) continues to be a primary intervention for multivessel coronary artery disease, using venous or arterial conduits to circumvent obstructed coronary vessels. In the United States, approximately 200,000 CABG procedures are conducted each year. Compared with percutaneous coronary intervention, CABG is favored in patients with advanced atherosclerosis, diabetes, and complex coronary anatomy. Despite advancements in surgical techniques and perioperative care, CABG continues to be associated with significant complications, including infection, stroke, renal failure, pneumonia, pulmonary embolism, pleural effusion, arrhythmias, prolonged ventilatory support, myocardial infarction, post-pericardiotomy syndrome, and delirium. The occurrence of these complications is contingent on pre-existing risk factors as well as intraoperative and postoperative variables. One significant postoperative complication is atrial fibrillation, which affects 16% to 50% of patients and typically manifests 2 to 4 days following surgery. Colchicine, an anti-inflammatory agent traditionally used in the treatment of gout, familial Mediterranean fever, and pericarditis, has emerged as a potential therapeutic option for mitigating inflammation-associated complications, such as postoperative atrial fibrillation (POAF). This review investigates the role of colchicine in the prevention of POAF following CABG, analyzing proposed mechanisms, relevant clinical trials, and potential clinical implications.

Urinary uric acid measurement is an important tool for clinical screening and differential diagnosis of diseases such as gout and hyperuricemia. To overcome the limitations of the traditional phosphotungstic acid colorimetric method which requires the use of expensive and bulky UV-Vis spectrophotometers, this study employed 3D photopolymerization printing technology to fabricate a hand-held visible spectrophotometer for the quantitative determination of uric acid concentration in human urine. The device integrates an LED light source, a bandpass filter, a 3D-printed detection cell, a silicon photodiode, and a high-precision voltmeter. Its analytical performance was evaluated using methylene blue and phosphate solutions, followed by quantitative determination of uric acid. The device is not only compact and portable but also low-cost. Within the appropriate concentration range, the device demonstrated excellent linear correlation (R[2] > 0.99) and a low relative standard deviation (RSD). Bland-Altman analysis confirmed the consistency of the measurement results with those obtained using a commercial UV-Vis spectrophotometer. Analysis of the recovery rates for the uric acid test kit revealed that recovery rates at low, medium, and high spiked concentrations ranged from 92% to 104%, and the relative standard deviation (RSD) from three replicate measurements was less than 5% in all cases, indicating high stability of the device. Furthermore, specificity tests conducted on three potential interferents present in urine demonstrated that the method possesses high specificity. This detection device enables rapid point-of-care testing (POCT) for uric acid levels in urine and holds broad application prospects in community clinics and home self-testing scenarios.

The bone marrow immune microenvironment (BMME) is a critical factor in multiple myeloma (MM) pathogenesis. Despite higher incidence of MM among self-identified African Americans, the relationship between African genetic similarity and the BMME remains unclear. We present the largest analysis to date assessing the impact of Ancestry on the BMME in myeloma (N=320, including 64 with ≥50% African genetic similarity, AFR-High) leveraging our recently generated Immune Atlas. AFR-High was associated with enrichment of late T-effector cells, driven by rare cytotoxic CD4[+] T cells, suggesting a distinct adaptive BMME. AFR-High exhibited expansion of late-differentiated adaptive NK cells with high cytotoxic GNLY and GZMH expression. AFR-High depicted reduced CD14[+] monocytes, increased CD16[+] non-classical monocytes, and expansion of macrophage-like monocyte populations with enrichment of metabolic adaptation, efferocytosis and phagocytic clearance programs, and immunoregulatory pathways. These findings reveal a shift from an innate inflammatory immune landscape toward adaptive cytotoxic and immunoregulatory remodeling associated with African genetic similarity in MM.

Cardiovascular diseases remain the leading cause of morbidity and mortality worldwide; however, effective clinical therapies that achieve myocardial regeneration are still lacking, underscoring the urgent need for novel therapeutic strategies. In this study, we identified an RNA-binding protein Ptbp1, a key component of RNA metabolism, as a critical regulator of cardiomyocyte proliferation via the formation of biomolecular condensates. We found that Ptbp1 exhibits granule-like structures in cardiomyocyte nuclei during fetal to early postnatal stages. These Ptbp1 foci are phase-separated liquid droplets formed via its multivalent RNA binding domains. Functional analyses revealed that Ptbp1 is essential for cardiomyocyte proliferation in neonatal mouse primary culture assays. Furthermore, proximity labeling using a primary antibody-based approach combined with RIP-seq in highly purified cardiomyocyte populations demonstrated that these condensates are enriched with multiple proliferation-associated factors. Our findings identify a novel phase-separated condensate in cardiomyocytes and provide a new potential therapeutic target for cardiac regeneration.

Gouty arthritis is characterized by monosodium urate (MSU) crystal deposition, persistent joint inflammation, oxidative stress, and limited drug penetration. Here, we report an injectable hydrogel system embedding asymmetric Janus nanomotors (Col-PLGA@Au-CU) that integrates enzymatic cascade reaction, photothermal propulsion, and on-demand drug release for active gout therapy. The nanomotors consist of colchicine-loaded PLGA cores partially coated with gold nanoshells and functionalized with uricase (UOx) and catalase (CAT), which are encapsulated in a chitosan-based hydrogel for intra-articular retention. Under near-infrared (NIR) irradiation, the gold nanoshells generate localized heat, which accelerates the release of the nanomotors from the hydrogel. The elevated temperature also enhances the UOx/CAT cascade reaction, resulting in increased oxygen generation and enhanced active motion of the nanomotors. Meanwhile, the photothermal effect accelerates the release of colchicine from the hydrogel. The enzymatic cascade not only depletes uric acid but also decomposes H2O2 into O2 and H2O, relieving oxidative stress and hypoxia. In vitro, the NIR-triggered nanomotors exhibited significantly enhanced cellular uptake, ROS scavenging, HIF-1α suppression, and M2 macrophage polarization. In a murine MSU-induced gout model, intra-articular injection of Col-PLGA@Au-CU@CS hydrogel followed by NIR irradiation effectively reduced joint swelling, restored gait patterns, decreased synovial inflammation, protected cartilage integrity, and downregulated TNF-α and IL-6 expression, without systemic toxicity. This enzyme-powered, photothermal-activatable Janus nanomotor hydrogel represents a controlled-release platform that combines enhanced active transport, microenvironment modulation, and triggered drug delivery, offering a promising strategy for precision therapy of gouty arthritis. STATEMENT OF SIGNIFICANCE: This study presents a novel injectable Janus nanomotor-integrated hydrogel (Col-PLGA@Au-CU@CS) for the treatment of gouty arthritis. By combining an enzymatic cascade (uricase and catalase) with a photothermal gold nanoshell, the system achieves simultaneous uric acid depletion, hydrogen peroxide decomposition, and NIR-triggered self-propulsion. The asymmetric nanomotors overcome poor drug penetration into avascular cartilage, while the hydrogel ensures intra-articular retention. Under NIR irradiation, enhanced directional motion, on-demand colchicine release, and reactive oxygen species scavenging lead to marked suppression of synovial inflammation, M2 macrophage polarization, and cartilage protection in a murine gout model. This work establishes an enzyme-powered, photothermal-activatable platform that integrates active tissue penetration, microenvironment modulation, and triggered drug delivery, offering a promising precision therapy strategy for gouty arthritis and potentially other inflammatory joint diseases.