Thyroid hormones (TH) are pivotal regulators of poultry growth and development. However, the effects of monochromatic light on thyroid function in broilers remain unclear. Therefore, newly hatched Arbor Acre (AA) broilers were randomly reared under white light (WL, 400-700 nm), red light (RL, 660 nm), green light (GL, 560 nm), and blue light (BL, 480 nm) until 42 days. The results showed that compared with WL, RL reduced thyroid weight and elevated serum free triiodothyronine (FT3) levels, whereas GL produced no significant alterations in thyroid weight or circulating TH levels. In contrast, BL increased thyroid weight and thyroid index and decreased serum triiodothyronine (T3) and FT3 concentrations. Furthermore, thyroid hormone synthesis-related genes were slightly upregulated in RL compared with WL, although these changes were not statistically significant. Conversely, BL downregulated the expression of thyroid hormone synthesis-related genes, including thyroid-stimulating hormone receptor (TshR), thyroid transcription factor 1 (Ttf1), sodium-iodide cotransporter (Nis), and thyroid peroxidase (Tpo), and decreased type 2 deiodinase (Dio2) protein expression. Moreover, endoplasmic reticulum (ER) stress-related markers were slightly decreased in RL but elevated in BL, which activated the PERK-eIF2α-ATF4-CHOP pathway and was associated with oxidative stress and increased Bax expression. These findings suggest that monochromatic light affects thyroid function in broilers, and BL exposure is associated with altered thyroid hormone synthesis and ER stress-related signaling.

A quantitative real-time polymerase chain reaction (qPCR)-based method was established and validated for the detection of residual host DNA in recombinant human C1 esterase inhibitor (rhC1INH), a biopharmaceutical produced in the mammary glands of transgenic rabbits. DNA was extracted from rhC1INH samples using a sodium iodide-based extraction kit, and a TaqMan qPCR assay targeting the rabbit-specific L1Oc gene was optimized to evaluate its specificity, linearity, limit of quantification (LOQ), accuracy, precision, and robustness. The method exhibited high species specificity, with no cross-reactivity to human or other common mammalian DNA. A broad dynamic range of 0.001-100 pg/μL was achieved, with the standard curve showing excellent linearity (R[2] > 0.99) and amplification efficiency of 90-110%. The LOQ was determined to be 0.001 pg/μL, satisfying the sensitivity requirements for trace DNA detection. Spike-and-recovery assays verified favorable quantification accuracy, with recovery rates ranging from 71.83% to 97.26% at low, medium, and high concentration levels. Intra-assay and inter-assay precision were assessed, and the relative standard deviation (RSD) was no more than 15.42% at all tested concentrations, which confirmed good method repeatability. Method robustness was validated by investigating the influences of different reagent batches and lysis temperature variations, with all corresponding indicators exhibited RSD values no higher than 30%. This qPCR method features high specificity, superior sensitivity, and convenient operation, and can serve as a reliable technical means for the quality control of rhC1INH and other transgenic rabbit mammary gland-derived biopharmaceuticals.

Developing fragmentation-locked polymeric carbon nitride with global-to-local electron allocation is crucial for enhancing its catalytic performance toward peroxymonosulfate (PMS) activation. Herein, we propose a sodium-ion-locked, iodide-induced structural memory strategy to synthesize fragmented polymeric carbon nitride (NI-PCN), which enables a continuous global-to-local electron allocation pathway for boosted PMS activation. Benefiting from this structural-electronic synergism, NI-PCN achieves 98% degradation of lornoxicam (LC) within 6 min (K = 0.5751 min[-1]), which is 19.3 times higher than that of pristine PCN. Experimental characterizations combined with density functional theory (DFT) calculations reveal that Na[+] incorporation globally lowers the work function of the carbon nitride framework, thereby promoting long-range electron migration. Meanwhile, the cyano-rich edges formed during fragmentation and Na[+] mediated electronic regulation synergistically promote local charge polarization and interfacial electron transfer to PMS molecules. This global-to-local electron allocation synergy facilitates O─O bond elongation and accelerates interfacial electron transfer, thus enabling efficient PMS activation. This work provides a new paradigm for the structural-electronic synergistic design of high-performance catalysts for PMS activation.

Constitutive activation of signal transducer and activator of transcription 3 (STAT3) is a hallmark of prostate cancer (PC) progression. Here, we investigated the anticancer effects of artesunate (ART) and its underlying mechanisms in PC. ART selectively reduced the viability of PC cells with minimal toxicity toward normal prostate cells by inducing apoptosis, as evidenced by increased sub-G1 accumulation, Annexin V/propidium iodide (PI)-positive cells, and DNA fragmentation. These effects were mediated by reactive oxygen species (ROS), as glutathione (GSH) and N-acetyl-l-cysteine (NAC) significantly reversed ART-induced cytotoxicity. ART also depleted intracellular GSH and reduced superoxide dismutase (SOD) expression, thereby enhancing oxidative stress. Inhibition of STAT3 by ART was reversed by sodium orthovanadate, implicating protein tyrosine phosphatases (PTPs) in this process. ART downregulated anti-apoptotic B-cell lymphoma-2 (Bcl-2) family proteins, suppressed C-X-C motif chemokine ligand 12 (CXCL12)-induced migration, and inhibited epithelial-mesenchymal transition (EMT) through ROS-dependent activation of Src homology region 2 domain-containing phosphatase-1 (SHP-1). In vivo, ART significantly inhibited prostate tumor xenograft growth, reduced oncogenic protein expression in tumors, and lowered serum interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels. Collectively, ART suppresses PC growth, survival, migration, and EMT by targeting the STAT3 and ROS/SHP-1 signaling pathways, supporting its potential as a therapeutic candidate for PC.

Most thyroid cancers are differentiated tumours with favourable outcomes, but a clinically important minority develops invasion, distant metastasis, loss of radioiodine uptake and histological dedifferentiation. TP53 encodes p53, a tumour suppressor that coordinates DNA-damage responses, cell-cycle arrest, apoptosis and genome stability. In thyroid cancer, TP53/p53 abnormalities show a stage-dependent pattern. They are uncommon in conventional low-risk differentiated thyroid cancer (DTC), but become enriched in high-grade DTC, poorly differentiated thyroid carcinoma, anaplastic thyroid carcinoma, radioiodine-refractory disease and rapidly progressive tumours. This Review integrates the 2022 WHO classification, the 2025 American Thyroid Association guideline, early pathology studies, modern genomic cohorts, mechanistic models and recent therapeutic evidence. Current data support TP53/p53 alteration as both a marker and a functional contributor to high-grade transformation and clonal progression. In radioiodine refractoriness, TP53 abnormality is best interpreted as part of a multistep progression background involving dedifferentiation and clonal selection, rather than as a single cause of iodine-uptake loss. Clinically, TP53 testing is most useful in high-risk, progressive or treatment-refractory disease and should be interpreted together with histology, radioiodine avidity, TERT, BRAF/RAS, PI3K/AKT alterations and treatment response.

Photoluminescent compounds showing distinct and selective optical response to external perturbation are essential components for sensing applications. Herein, we present a copper(I) iodide-sodium luminescent complex assembled with a hybrid phosphane-phosphinate ligand. The photoemission of the tetrametallic {Cu2I2Na2} aggregate is consistent with the thermally activated delayed fluorescence that originates from the [CuI(phosphane)] motifs but strongly depends on the coordination environment of sodium ions completed by O-donor solvent molecules, Na-π(phenyl) interactions, and/or Na-I bonds. The reversible removal and vapor-phase addition of methanol, ethanol, water, and dimethoxyethane as Na-bound ligands alter the solid-state luminescence from blue (461 nm) to yellow (570 nm) with quantum yields reaching 0.73. Importantly, different photoemission responses to methanol (522 nm) and ethanol (492 nm) are complemented by preferred binding of methanol and its detection in up to 1:10 methanol:ethanol mixtures. Variations of luminescence among the studied solvates are attributed to the alterations of secondary sphere interactions involving sodium ions and illustrate a new approach to stimuli-responsive metal complexes constructed from soft-hard donor ligands.

Information in this record refers to the use of sodium iodide I 131 as a diagnostic and therapeutic agent. The use of I 131 is contraindicated during lactation. Breastfeeding should be discontinued permanently for this child after administration of sodium iodide I 131 in a dose of 0.01 MBq (0.004 mCi) or greater to a nursing mother.[1-7] Ceasing breastfeeding 4 to 6 weeks before receiving a therapeutic dose of sodium iodide I 131 is recommended to reduce the radiation dose to the breasts and the risk of milk leakage that can contaminate clothing with radioactive iodine.[8-10] The American Thyroid Association recommends using I 123 or Tc99m pertechnetate scans for diagnosis of hyperthyroidism in nursing mothers.[1] Parents should refrain from close contact with their infants after therapeutic iodine 131 administration. The exact duration depends on the dose administered, condition being treated, and source of the recommendation.[11,12] Recommended times range from 15 to 27 days after hyperthyroidism treatment, 16 to 24 days after ablation of thyroid cancer, and 4 to 5 days after follow-up therapy of thyroid ablation therapy.[12] Nursing mothers should not work with substances containing I 131 in their workplace.[13]

Sediments in river estuarine systems facilitate the long-term accumulation of naturally occurring radionuclides, playing a critical role in controlling their environmental distribution and potential radiological exposure pathways. This study presents a gamma-spectrometric assessment of natural radionuclides ([40]K, [238]U, and [232]Th) in estuarine sediments within a tropical river system where both natural geological processes and human activities occur. The sediments were quantified using a calibrated sodium iodide gamma-ray spectrometer, and standard radiological hazard indices were evaluated to assess potential environmental and human health risks. The mean activity concentrations were 490.50 i7.66 Bq/kg ([40]K), 5.67 , 0.20 Bq/kg ([238]U), and 4.81),0.26 Bq/kg ([232]Th). While [40]K actively slightly exceeded the UNSCEAR average by 16.79%, the [238]U and [232]Th concentrations were 82.82% and 89.31%, respectively, below the global thresholds. Derived radiological parameters, including radium equivalent activity (50.32 Bq/kg), dose rate (26.13 nGy/h), annual effective dose (0.03 mSv/y), and annual gonadal dose (191.64 µSv/y), were all within internationally accepted safety thresholds. The results suggest that sediment-associated radionuclides in the studied estuarine environment do not pose significant radiological risks through external exposure pathways. These findings contribute baseline data for tropical estuarine sediment systems and support comparative radiological assessments across similar depositional environments globally.

Radioiodine therapy of differentiated thyroid cancer is effective and possibly curative in patients with metastatic lesions that retain iodine avidity. However, in clinical practice, iodine avidity in any metastatic site is usually unknown at the point of initial treatment. Avidity prediction could enable more tailored initial radioiodine treatment. This work aimed to establish the best predictive factors for iodine avidity and subsequent treatment response. Thirty-one patients with metastatic or recurrent thyroid cancer sites in which iodine avidity could be assessed by image-based analysis were included. In tissue specimens from primary surgery, immunohistochemical expression of thyroglobulin (Tg), thyroid peroxidase (TPO), sodium-iodide symporter (NIS) and Ki67, and mutational status of BRAF, RAS and the TERT promoter was analyzed. Biochemical and structural response were assessed by serum Tg response and radiological evaluation. High-risk histology (widely invasive follicular, tall cell subtype papillary, differentiated high-grade or poorly differentiated thyroid carcinoma) combined with expression of TPO, Tg and cytoplasmic NIS performed well in predicting treatment response and iodine avidity. Approximately half of the variation between patients was explained by those variables, outperforming pT stage and mutational status. TPO and Tg expression were the largest contributors in prediction modelling. Radioiodine treatment response and iodine avidity in thyroid cancer can be predicted from histopathological analysis of the primary tumor. High-risk histology and expression of TPO, Tg and NIS were robust and informative predictors. This may be used to adapt treatment strategy in adjuvant and metastatic therapy settings.

Bacterial infections of biofilms are hard to treat as the matrix and physiological differences in the cells within a biofilm limit the ability of traditional antibiotics to control the growth of bacteria. We synthesized a sodium butyrate-encapsulated manganese tetrakis (4-carboxyphenyl) porphyrin hydrogen-bonded organic framework (NaB@Mn-TCPP HOF), which was used to determine its physical and chemical properties, guest-loading capacity, release behavior, hemolytic effects, antibacterial activity and anti-biofilm formation of Escherichia coli and Staphylococcus aureus. The NaB incorporation was confirmed by Fourier-transform infrared spectroscopy, powder X-ray diffraction, ultraviolet-visible spectroscopy, dynamic light scattering, zeta-potential measurement, elemental mapping, and other methods demonstrated that the parent Mn-TCPP HOF retained most of its principal spectroscopic, solid-state diffraction, and colloidal features. Indirect spectrophotometry of absorbance of UV light revealed an apparent loading of NaB of 56 percent with respect to the mass of carrier at feed ratio of 4 mg NaB per 5 mg carrier corresponding to an estimated NaB content of about 36 wt% in the recovered composite and an apparent encapsulation rate of about 70%. About half of the calculated loaded NaB was released gradually over 12 h without reaching the final plateau. In a five-group design that is exploratory and not dose-matched, images of the colonies were taken after exposure to 660 nm irradiation at 100 mW cm[-2,] and the results indicated the reduction of colony development, crystal-violet staining, propidium-iodide-associated signal, and surface-related bacterial coverage in the NaB@Mn-TCPP HOF group. Biofilm experiment was performed on the inhibition of a new biofilm in the course of 24 h instead of destroying an already matured one. After 2 hours of exposure, less than 5 percent hemolysis was produced by the composite at 100 micrograms mL [-1]. These findings can be used to make further studies of NaB@Mn-TCPP HOF as a combined material platform that reacts to light. It has not been clarified by the current design whether reactive oxygen species, manganese excretion, the pathway of bacteria controlled by NaB, or pharmacological interactions were involved.