Sulfur mustard (SM), a chemical warfare agent, has been linked to chronic health issues, including thyroid dysfunction. This study investigates the impact of SM exposure on thyroid function indices in men and women veterans, exploring sex-based differences and correlations with injury severity. A cross-sectional study was conducted involving 412 SM-exposed veterans (315 men, 97 women) and 113 healthy controls (79 men, 34 women). Participants were categorized by injury severity into three subgroups: 5%-10%, 15%-35%, and > 35%. Thyroid function indices (triiodothyronine (T3), thyroxine (T4), thyroid-stimulating hormone (TSH), thyroglobulin (TG), anti-thyroglobulin antibodies (anti-TG), and anti-thyroid peroxidase antibodies (anti-TPO), and T3 uptake) were measured. TSH and T3 uptake levels were significantly higher in SM-exposed women than in controls. In men, TG levels were significantly higher than in women in both SM-exposed and control groups, while anti-TG levels were lower. Additionally, anti-TPO levels were elevated in SM-exposed men compared with control men and SM-exposed women. TG levels increased in men across all injury severities compared with controls, with anti-TG levels decreased in SM-exposed men at all severities. Women showed elevated T3 uptake and TSH levels across all severities compared with controls. Effect size analysis confirmed significant increases of T3 uptake in women and TG levels in men. This study highlights sex-specific differences in thyroid dysfunction among SM-exposed veterans, with women showing signs of hypothyroidism and men exhibiting autoimmune responses. Injury severity further exacerbated these effects, emphasizing the need for gender-specific monitoring and intervention strategies for SM-exposed individuals.

The stability of inorganic CsPbI3 perovskite solar cells (IPSCs) has been greatly limited by their accelerated degradation in a high-humidity environment. In this investigation, we design a defect-passivation approach using monodentate p-toluenesulfonyl hydrazide (TSH) and a bidentate ligand, 2-amino-6-methoxybenzothiazole (AMBT), which boosts the humidity resistance of CsPbI3 perovskite under 80% relative humidity (RH). Based on density-functional-theory calculations, it has been found that AMBT has a significantly higher binding energy of -1.91 eV with respect to CsPbI3 than that of TSH with a binding energy of -0.98 eV, consistent with their extremely stable Pb-N and Pb─O coordination bonds, ascertained by XPS and FTIR spectroscopy. Surface modification of AMBT effectively promotes crystal perfection, decreases trap state, and extends carrier lifetime, yielding a maximum power conversion efficiency (PCE) of 18.52% with a high fill factor of 84.35%. Unencapsulated device structures with 80% RH maintain their β-phase structure for over 60 min, and corresponding IPSCs maintain 40% of their initial efficiency over 10 days, being among the highest humidity-resistance strengths for CsPbI3 perovskite-based devices. Our results provide a powerful strategy for developing moisture-independent CsPbI3 perovskite solar cells.

Dexamethasone induces systemic toxicity, including oxidative stress, inflammation, hematological disturbances, and organ damage, particularly in the lungs and thyroid. Taurine exhibits antioxidant and anti-inflammatory properties, but poor bioavailability limits its efficacy. Nanoparticle delivery may enhance stability and tissue targeting. This study aimed to evaluate the protective effects of taurine-loaded chitosan nanoparticles (Tau-CS NPs) against dexamethasone-induced tissue injury in rats. Forty-eight male Wistar rats were allocated into control, DEXA, DEXA + silymarin, DEXA + taurine, and DEXA + Tau-CS NPs groups. Tau-CS NPs were characterized by TEM, UV-vis, FTIR, encapsulation efficiency, and drug loading. Hematology, oxidative stress markers (CAT, SOD, GSH, MDA), thyroid hormones (T3, T4, TSH, calcitonin), protein profile, lung and thyroid histopathology, and MPO expression were assessed. Tau-CS NPs showed uniform spherical morphology (11-60 nm), high encapsulation (98.2%), and substantial loading (50.36%). Dexamethasone caused hematological, oxidative, thyroidal, and histological disturbances. Tau-CS NPs markedly restored hematological indices, antioxidant defenses, thyroid function, protein profile, and tissue architecture, outperforming free taurine and silymarin. MPO expression was significantly reduced, indicating decreased inflammation. Taurine nanoparticles effectively mitigate dexamethasone-induced systemic and organ-specific toxicity, offering improved bioavailability and targeted delivery, highlighting their therapeutic potential.

Tirzepatide, a dual glucagon-like peptide-1 (GLP-1)/glucose-dependent insulinotropic polypeptide (GIP) receptor agonist, is increasingly prescribed for obesity and glycemic control. Its effects on gastric emptying, appetite regulation, and rapid weight loss may influence thyroid hormone homeostasis and the pharmacokinetics of narrow-therapeutic-index medications such as levothyroxine. Emerging clinical experience suggests that GLP-1-based therapies can suppress thyroid-stimulating hormone (TSH), alter thyroid hormone dynamics, and precipitate symptoms of thyrotoxicosis in patients receiving thyroid hormone replacement. As use of incretin therapies expands, understanding their potential interaction with thyroid physiology is increasingly important. We describe a 52-year-old woman with a history of thyroidectomy complicated by postoperative hypothyroidism, maintained on stable doses of levothyroxine for several years. After six months of tirzepatide therapy, she experienced 48 pounds of intentional weight loss and developed dizziness, tachycardia, weakness, and confusion. Laboratory evaluation showed a markedly suppressed TSH and elevated free T4, consistent with significant over-replacement with levothyroxine. She required emergent dose reduction and supportive care, with gradual resolution of symptoms after adjustment of her thyroid regimen. Key contributing factors included substantial weight loss without proportional levothyroxine dose reduction, delayed gastric emptying altering levothyroxine absorption, and absence of endogenous thyroid reserve following thyroidectomy. These changes created a clinical environment highly susceptible to pharmacologic fluctuations and rapid shifts into iatrogenic thyrotoxicosis. Additionally, GLP-1 therapy-associated decreases in blood pressure and appetite likely amplified her acute presentation. This case highlights the importance of vigilant monitoring in post-thyroidectomy patients who begin tirzepatide or other incretin-based medications. Clinicians should anticipate the need for levothyroxine dose adjustments as weight decreases and gastrointestinal motility changes. Early follow-up, routine thyroid function testing, and prompt evaluation of new cardiovascular or neurocognitive symptoms are essential to prevent avoidable morbidity related to drug-hormone interactions.

Cold exposure is an unavoidable stressor in cold regions, leading to growth retardation, oxidative damage, and endocrine disruption. This study investigated changes in blood parameters and antioxidant function in the brown adipose tissue (BAT) of mice exposed to cold. Sixteen naturally mated female mice (aged 70 days) were selected and divided into a control group (CON, n = 8, 25 ± 1 °C) and a cold exposure group (CE, n = 8, 4 ± 1 °C). Each pregnant female gave birth to approximately 12 pups, and the litter (dams and pups co-housed) served as the independent experimental unit, with both euthanized for sampling when the pups reached 20 days of age. Results showed that cold exposure increased ADFI and ADG but decreased the feed conversion rate (FCR) in lactating mice. It also decreased platelet count (PLT) and mean corpuscular hemoglobin concentration (MCHC), elevated lactate dehydrogenase (LDH) activity, and decreased TG and non-esterified fatty acid (NEFA) levels. Hormonal changes included increased adrenocorticotropic hormone (ACTH), apelin 12 (AP12), INS, NE, decreased cortisol (COR), LEP, and thyroid-stimulating hormone (TSH). In pups, cold exposure inhibited growth, reduced PLT, plateletcrit (PCT), red blood cells (RBC), and hemoglobin (HGB), altered lipid profiles, and induced hormonal shifts. Notably, cold exposure enhanced the BAT antioxidant capacity in pups, increasing the total antioxidant capacity (T-AOC) and antioxidant enzyme activities, as supported by gene expression. These findings suggest that, despite growth suppression, mice maintain homeostasis by modulating blood parameters and enhancing BAT antioxidant function to mitigate cold-induced damage.