Urine-free response criteria predict progression-free survival in multiple myeloma: a post hoc analysis of BMT CTN 0702
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Urine electrooxidation for energy–saving hydrogen generation
Urea electrooxidation offers a cost-effective alternative to water oxidation for energy-saving hydrogen production. However, its practical application is limited by expensive urea reactants and sluggish reaction kinetics. Here, we present an efficient urine electrolysis system for hydrogen production, using cost-free urine as feedstock. Our system leverages a discovered Cl-mediated urea oxidation mechanism on Pt catalysts, where adsorbed Cl directly couple with urea to form N-chlorourea intermediates, which are then converted into N2 via intermolecular N–N coupling. This rapid mediated-oxidation process notably improves the activity and stability of urine electrolysis while avoiding Cl-induced corrosion, enabling over 200 hours of operation at reduced voltages. Accordingly, a notable reduction in the electricity consumption is achieved during urine electrolysis (4.05 kWh Nm−3) at 300 mA cm−2 in practical electrolyser for hydrogen production, outperforming the traditional urea (5.62 kWh Nm−3) and water (4.70–5.00 kWh Nm−3) electrolysis.
Golgi-restored vesicular replenishment retards bone aging and empowers aging bone regeneration
Healthy aging is a common goal for humanity and society, and one key to achieving it is the rejuvenation of senescent resident stem cells and empowerment of aging organ regeneration. However, the mechanistic understandings of stem cell senescence and the potential strategies to counteract it remain elusive. Here, we reveal that the aging bone microenvironment impairs the Golgi apparatus thus diminishing mesenchymal stem cell (MSC) function and regeneration. Interestingly, replenishment of cell aggregates-derived extracellular vesicles (CA-EVs) rescues Golgi dysfunction and empowers senescent MSCs through the Golgi regulatory protein Syntaxin 5. Importantly, in vivo administration of CA-EVs significantly enhanced the bone defect repair rate and improved bone mass in aging mice, suggesting their therapeutic value for treating age-related osteoporosis and promoting bone regeneration. Collectively, our findings provide insights into Golgi regulation in stem cell senescence and bone aging, which further highlight CA-EVs as a potential rejuvenative approach for aging bone regeneration.
Derivation of human toxicokinetic parameters and internal threshold of toxicological concern for tenuazonic acid through a human intervention trial and hierarchical Bayesian population modeling
Tenuazonic acid (TeA), a mycotoxin produced by Alternaria alternata, contaminates various food commodities and is known to cause acute and chronic health effects. However, the lack of human toxicokinetic (TK) data and the reliance on external exposure estimates have stalled a comprehensive risk assessment for TeA.
Young infants’ exposure to parabens: lotion use as a potential source of exposure
Parabens are widely used as antimicrobials in personal care products and pharmaceuticals. While previous studies demonstrate paraben exposure is ubiquitous, data investigating infants’ exposure is limited.
Gene therapy of Dent disease type 1 in newborn ClC-5 null mice for sustained transgene expression and gene therapy effects
Dent disease type 1 is caused by changes in the chloride voltage-gated channel 5 (CLCN5) gene on chromosome X, resulting in the lack or dysfunction of chloride channel ClC-5. Individuals affected by Dent disease type 1 show proteinuria and hypercalciuria. Previously we found that lentiviral vector-mediated hCLCN5 cDNA supplementary therapy in ClC-5 null mice was effective only for three months following gene delivery, and the therapeutic effects disappeared four months after treatment, most likely due to immune responses to the ClC-5 proteins expressed in the treated cells. Here we tried two strategies to reduce possible immune responses: 1) confining the expression of ClC-5 expression to the tubular cells with tubule-specific Npt2a and Sglt2 promoters, and 2) performing gene therapy in newborn mutant mice whose immune system has not fully developed. We found that although Npt2a and Sglt2 promoters successfully drove ClC-5 expression in the kidneys of the mutant mice, the treatment did not ameliorate the phenotypes. However, gene delivery to the kidneys of newborn Clcn5 mutant mice enabled long-term transgene expression and phenotype improvement. Our data suggest that performing gene therapy on Dent disease affected subjects soon after birth could be a promising strategy to attenuate immune responses in Dent disease type 1 gene therapy.
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