Electrochemical determination of aspirin using a poly(alizarin red S) modified glassy carbon electrode in pharmaceutical formulations

Bile duct carcinoma (BDC) is a highly aggressive malignancy. While epidemiological evidence suggests that acetylsalicylic acid (ASA [aspirin]) reduces BDC risk, the underlying molecular mechanisms have not been fully elucidated. This investigation explored the antineoplastic mechanisms of ASA in BDC cells. The human BDC cell line SNU-245 was used in all experiments. Cell viability was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, whereas apoptosis and caspase-3 levels were evaluated using enzyme-linked immunosorbent assay. Protein expression was analyzed using Western blotting and immunofluorescence. Functional pathway interactions were investigated using siRNA-mediated gene silencing. ASA reduced cell viability and increased apoptosis markers, accompanied by increased Bax and p53 expression and decreased Bcl-2 levels. ASA treatment reduced cyclooxygenase-2 (COX-2) expression and decreased epidermal growth factor receptor (EGFR)levels. COX-2 knockdown markedly attenuated deoxycholic acid (DCA)-induced EGFR phosphorylation, whereas EGFR silencing partially reduced DCA-induced COX-2 expression. These results suggest reciprocal signaling interactions, with COX-2 exerting a relatively stronger upstream influence. ASA increased phosphorylation of AMP-activated protein kinase at threonine 172 (AMPKᵀʰʳ¹⁷²) and reduced insulin like growth factor-1 receptor (IGF-1R)/insulin receptor substrate-1 (IRS-1) signaling and decreased mammalian target of rapamycin (mTOR) phosphorylation. ASA also attenuated epidermal growth factor (EGF)-induced changes in epithelial-mesenchymal transition- related markers, including preservation of E-cadherin and reduction of N-cadherin expression. In this in vitro model, ASA exposure was associated with coordinated modulation of multiple cell-survival-related signaling pathways in BDC cells, including COX-2/EGFR signaling, AMPK activation, and IGF-1R-mediated mTOR regulation. These findings provide mechanistic insight into the potential antineoplastic effects of ASA and support further translational studies in BDC.

ABSTRACT The aim of this work is to investigate the adsorption of Aspirin or Acetylsalicylic acid (ASA) present in an aqueous solution, on SiO 2 , TiO 2 , and TiO 2 /SiO 2 nanostructures. TiO 2 /SiO 2 nanostructures were synthesized using rice husk ash (RHA) as the SiO 2 source and titanium tetrachloride (TiCl 4 ) as a precursor for TiO 2 . Nanostructures of TiO 2 , SiO 2 , and TiO 2 /SiO 2 , using XRD, FT‐IR, BET, SEM, and Zeta Potential equipment, were characterized. The effect of pH (pH 1, 4, 7, 12), initial ASA concentration (3.5‐5.5 ppm), temperature (25°C, 35°C, 50°C), adsorbent dose (0.1‐3.0 g L −1 ), and adsorption time (0‐24 h) on the adsorption process has been examined. The most favorable adsorption of ASA was observed at acidic pH, that is especially pH 4. Using an initial concentration of 5.5 ppm ASA solution and a dose of 0.75 g L −1 SiO 2 , TiO 2 , and TiO 2 /SiO 2 nanostructures, the maximum removal of ASA was 38.08%, 21.89%, and 23.83%, respectively. Experimental data were fitted to the Langmuir (LIM), Freundlich (FIM), Tempkin (TIM), and Dubinin‐Radushkevic (DRIM) adsorption isotherm models. The two‐parameter isotherms that provide the best match and have the highest correlation coefficient are, in order of precision: LIM > FIM > TIM > DRIM. Maximum adsorption capacities ( q m ) of SiO 2 , TiO 2 , and TiO 2 /SiO 2 were calculated as 3.42, 2.81, and 3.35 mg g − 1 , respectively. To test the data obtained from these isotherm models, several error functions, that is Marquardt's Percent Standard Deviation (MPSD), Hybrid error function (HYBRID), Sum of the Absolute Errors (SAE), Average Relative Error percentage (ARE), and Sum of Square Error (SSE), were also used. As all error functions are compared, the Langmuir (LIM) adsorption isotherm model fits the experimental data quite well. Adsorption kinetics of ASA was performed with pseudo‐first‐order (PFOM), pseudo‐second‐order (PSOM), Elovich (EM), and Weber‐Morris (WMM) models. Pseudo‐second‐order model, PSOM (R 2 = 0.995‐0.998) is found to be the most compatible with the experimental data. Thermodynamic studies on ASA removal elucidated that ASA removal using TiO 2 as an adsorbent is an exothermic and spontaneous process, while it is endothermic and nonspontaneous when SiO 2 or TiO 2 /SiO 2 is used as an adsorbent.

Background: Nonsteroidal anti-inflammatory drugs (NSAID) are the second most frequent cause of drug-induced hypersensitivity after β-lactam antibiotics. Diagnosing cross-intolerance reactions to NSAIDs remains challenging because conventional allergy tests are not useful and drug provocation tests (DPT), the current criterion standard, are resource-intensive and carry risk of severe reactions. Basophil activation testing (BAT) has emerged as a potential ex vivo diagnostic alternative. Objective: This study aimed to evaluate the diagnostic utility of the BAT for cross-intolerance reactions to NSAIDs among Vietnamese patients, including the identification of optimal drug type, concentration, and cutoff values. Methods: This validation study used a case-control design that involved 38 patients previously diagnosed with cross-intolerance to NSAIDs and 34 healthy controls. The diagnosis of NSAID cross-intolerance was established according to the international consensus guidelines, based on a detailed clinical history and, when indicated, a DPT. Both groups underwent BAT by using two NSAIDs at two concentrations each: acetylsalicylic acid (ASA) at 1.25 mg/mL and 0.5 mg/mL, and ketorolac at 1.25 mg/mL and 0.5 mg/mL. Flow cytometric analysis was performed to assess basophil activation based on CD63 and CD203c expression. Results: ASA 1.25 mg/mL showed the best BAT diagnostic performance for cross-intolerance, achieving 55.3% sensitivity and 91.2% specificity by using cutoffs of ≥4% activated basophils and stimulation index (SI) ≥ 1.5. Conclusion: BAT demonstrates moderate sensitivity but high specificity for NSAID cross-intolerance, particularly when ASA is used as the stimulant. These findings support BAT as a complementary confirmatory tool in selected patients at high risk, although negative results do not exclude hypersensitivity and DPT remains necessary when diagnostic confirmation is required. Further validation in clinically relevant populations is needed before routine clinical implementation.

Two randomized trials, the ALONE-AF and OCEAN, have provided valuable evidence to guide the management of oral anticoagulation therapy after ablation of atrial fibrillation. In the ALONE-AF study, amongst patients with no documented atrial fibrillation recurrence at 1 year after transcatheter ablation, the 2-year incidence of the composite endpoint of stroke, systemic embolism, and major bleeding was significantly lower in those who discontinued oral anticoagulation compared with those who continued therapy. This difference was driven by a reduction in major bleeding events, with similar rates of stroke between groups. In the OCEAN study, amongst patients without atrial fibrillation (AF) recurrence during the year following transcatheter ablation, rivaroxaban 15 mg, compared with acetylsalicylic acid (ASA), did not significantly reduce the 3-year incidence of stroke, systemic embolism, or new silent embolic cerebral infarction, but was associated with an increased risk of clinically relevant non-major bleeding. The annualized incidence of thromboembolic events was low (0.3-0.6 events per 100 patient-years). Taken together, data from these two trials suggest that discontinuation of oral anticoagulation (OAC) may be a clinically reasonable option in patients without AF recurrence for at least 1 year after ablation. This strategy should be limited to patients at low thromboembolic risk, comparable to those enrolled in the two trials. Furthermore, the implementation of optimal and sustainable rhythmmonitoring strategies is essential to support decisions regarding OAC discontinuation after AF ablation.

Dual antiplatelet therapy (DAPT) with acetylsalicylic acid (ASA) and a P2Y12 receptor inhibitor (P2Y12i) for 12 months represents the standard of care after acute coronary syndrome (ACS). However, balancing ischaemic protection against bleeding risk remains challenging, providing the rationale for the development of de-escalation strategies. European and U.S. guidelines allow shortening the duration of DAPT in patients at high bleeding risk, whilst still maintaining 12 months as the reference recommendation. Interest in abbreviated DAPT regimens has been driven by improvements in percutaneous coronary intervention devices and techniques, as well as by a better understanding of the temporal evolution of ischaemic and bleeding risks. Several trials have shown that short-duration DAPT followed by monotherapy-particularly with a P2Y12i-is not inferior in terms of ischaemic outcomes and significantly reduces bleeding events. In this context, the NEO-MINDSET trial failed to demonstrate the non-inferiority of immediate P2Y12i monotherapy compared with standard DAPT. In contrast, the TARGET-FIRST study confirmed the safety of ASA discontinuation after 30 days in selected patients, with a clear bleeding benefit. Overall, the available evidence indicates that immediate discontinuation of ASA in patients with acute coronary syndrome is not universally safe, whereas strategies based on at least 1 month of DAPT followed by monotherapy with a potent P2Y12i currently represent the most balanced approach for selected patients. More refined personalization of antiplatelet therapy, guided by an integrated assessment of ischaemic and bleeding risks, represents the future perspective in this field.

Significance of 8-iso-PGF2α in cardiovascular diseases.

Background: In the paediatric intensive care unit (PICU), certain drugs should be avoided or administered with strict precautions and close monitoring. This is due to their potential for toxicity or adverse effects or a lack of safety data, especially for critically ill children with organ failure. Additionally, practitioners must assess the unique pharmacokinetic and pharmacodynamic properties of drugs when treating critically ill children. In this narrative review, we highlight the risks, advantages, and disadvantages of three exemplary cases of drugs for paediatric patients hospitalised in the PICU: chloramphenicol, acetylsalicylic acid, and propofol. Methods: Apart from key papers on these drugs, a retrospective analysis of the English literature on chloramphenicol, acetylsalicylic acid (ASA), and propofol was performed on PubMed for papers from January 2014 to December 2025. Results: Chloramphenicol should be avoided in neonates due to the risk of grey baby syndrome. Acetylsalicylic acid (ASA) is contraindicated in children ≤18 years with suspected viral illness because of the risk of Reye's syndrome, but remains essential for Kawasaki disease and post-cardiac surgery antiplatelet therapy. Propofol should be avoided when used for a longer period at high doses. With proper dosing and monitoring, propofol-related infusion syndrome (PRIS) is preventable, but high-risk patients should receive alternative treatment. Conclusions: This narrative review highlights the significant risks associated with the use of chloramphenicol, ASA, and propofol in paediatric intensive care settings. Their potential for life-threatening and severe adverse reactions emphasises the need for cautious and informed use. Clinicians must carefully consider the risks and benefits of these drugs. To minimise adverse events, strict monitoring, dose adjustments, and the use of safer alternatives are essential. However, it appears that their use in well-defined circumstances in acute illness in children is still warranted. The findings of this narrative review underscore the need for further research to focus on identifying high-risk biomarkers, genetic predispositions, and safer alternatives to improve evidence-based guidelines and reduce morbidity and mortality in paediatric intensive care.

Pregnancy induces a hypercoagulable state peaking at delivery and reverting postpartum. This prospective cohort study evaluated the longitudinal progression of endogenous thrombin potential in 102 high-risk pregnant women in relation to the development of preeclampsia or gestational diabetes mellitus. Samples were collected from gestational weeks 8-15, with follow-ups every 2-12 weeks, and thrombin generation was assessed using Calibrated Automated Thrombography. Eleven women developed preeclampsia, and 19 developed gestational diabetes mellitus. Endogenous thrombin potential values were significantly elevated in patients who developed preeclampsia (2220 ± 357 nM*min, p < 0.001) or gestational diabetes mellitus (2298 ± 377 nM*min, p < 0.001) compared to the rest of the cohort (1995 ± 337 nM*min), with high levels evident from the first trimester-well before clinical symptoms. Notably, preeclampsia patients on acetylsalicylic acid therapy did not show further increases in endogenous thrombin potential, and acetylsalicylic acid intake in gestational diabetes mellitus patients effectively moderated endogenous thrombin potential progression. These findings suggest that higher early-pregnancy endogenous thrombin potential reflects an underlying hemostatic imbalance associated with the subsequent development of preeclampsia and gestational diabetes mellitus. Furthermore, acetylsalicylic acid appears to exert effects beyond its anti-inflammatory properties by moderating endogenous thrombin potential, providing new insights into the early pathophysiology and therapeutic modulation of high-risk pregnancies.

This study evaluated the anti-inflammatory potential of the acetone extract of green coffee beans (Coffea excelsa) using in vitro assays. The extract was assessed for its ability to inhibit protein denaturation and stabilize biological membranes using heat-induced hemolysis of human erythrocytes as a model. The extract exhibited an overall increase in inhibitory effect across the tested concentrations in both assays. In the protein denaturation assay, percentage inhibition increased from 13.10% at 100 µg/mL to 70.45% at 1000 µg/mL, with an IC₅₀ value of 249.8 µg/mL. Similarly, in the membrane stabilization assay, inhibition ranged from 21.16% to 62.06% across the same concentration range, with an IC₅₀ value of 391.6 µg/mL. Statistical analysis using one-way ANOVA followed by Dunnett’s post hoc test indicated that all tested concentrations produced significant effects compared to the control (p &lt; 0.0001). IC₅₀ values were determined using nonlinear regression analysis (n = 3). Although the extract showed lower activity compared with acetylsalicylic acid, it demonstrated moderate anti-inflammatory activity. These effects may be associated with the presence of bioactive compounds such as phenolics and flavonoids; however, this cannot be confirmed since no phytochemical analysis was conducted in this study. Overall, these results indicate that the acetone extract of green coffee beans possesses measurable anti-inflammatory properties in vitro, suggesting that it may serve as a potential source of bioactive compounds for further investigation. Further studies, including phytochemical characterization and in vivo evaluations, are required to validate these findings.

Thrombocytopenia remains a significant problem in patients with cardiovascular disease (CVD) due to the indispensable use of antiplatelet therapy. The aim of this study was to establish a novel flow cytometry (FC)-based method for measuring platelet reactivity during dual antiplatelet therapy (DAPT) and to compare it with impedance aggregometry (IA) in thrombocytopenic patients undergoing percutaneous coronary intervention (PCI). This prospective cross-sectional study included 30 patients with thrombocytopenia. Platelet aggregation was assessed using IA and FC. A similar response to arachidonic acid (AA), reflecting the effect of acetylsalicylic acid (ASA), was observed in both groups. Responses to thrombin receptor agonist peptide (TRAP) and adenosine diphosphate (ADP), measured with aggregometry, were significantly higher in thrombocytopenic patients than in patients with normal platelet counts. When the FC method was used, the response to AA was significantly higher in thrombocytopenic patients. The optimal cut-off value for the FC method to define adequate platelet reactivity inhibition with clopidogrel in thrombocytopenic patients was <25.7%. In patients with thrombocytopenia, IA is useful for assessing ASA response, whereas the presented FC method may be more accurate for evaluating response to clopidogrel.

This study aims to evaluate the medication use of patients hospitalized in the cardiology ward with different chronic conditions in addition to cardiovascular disease and to identify potential medication errors. The study included 110 patients who were admitted to the cardiology service of a public hospital in eastern Turkey, who were hospitalized for at least two days and who had additional chronic diseases. Information from the patients' medical records was analyzed and the diagnoses received during hospitalization were evaluated. Acute coronary syndrome (33.6%) was the most common reason for hospitalization, while 90% of the patients had hypertension. A total of 1061 drugs were prescribed to the patients participating in the study, with the most commonly prescribed drugs and drug groups being beta-blockers, proton pump inhibitors and antiplatelet agents. All drugs were evaluated for drug interactions and 1024 drug interactions were identified. The most common drugs found in interactions were acetylsalicylic acid and beta-blockers. A total of 89 criteria non-compliances were found in 42 patients evaluated under STOPP/START criteria. As a result of the medication appropriateness index analysis, the mean score of the medications was 9.89. Cardiovascular diseases are common diseases in the community and usually require the use of multiple drugs, so drug interactions are more common. It is important to evaluate the risk of drug interactions in patients using multiple drugs and to plan regular follow-up of patients due to possible side effects.

Coronary artery disease (CAD) remains a leading cause of mortality, and its frequent coexistence with atrial fibrillation (AF) significantly worsens prognosis, presenting physicians with a complex choice between stroke prevention, protection from coronary events, and minimization of bleeding risk. Even in patients with stable CAD, a high residual risk of thrombotic complications persists, driven by ongoing activation of the coagulation cascade, which traditional antiplatelet monotherapy cannot fully control. The strategy of dual pathway inhibition of thrombus formation has improved treatment outcomes: adding rivaroxaban at a "vascular" dose of 2.5 mg twice daily to acetylsalicylic acid provides a significant reduction in the risk of cardiovascular death and ischemic events with an acceptable safety profile. This approach is justified in patients at high ischemic risk, particularly those with a history of myocardial infarction or multivessel CAD. In the presence of AF, the principles of antithrombotic protection fundamentally change, mandating the inclusion of full-dose anticoagulation. The key strategy to address this challenge is treatment de-escalation: from the shortest possible courses of triple therapy (anticoagulant plus two antiplatelet agents) in the acute phase after percutaneous coronary intervention to dual therapy (anticoagulant plus clopidogrel) during the first year of follow-up. In the long term, stable patients benefit from a transition to anticoagulant monotherapy, which is non-inferior to combination therapy in preventing thrombotic events and significantly superior in terms of safety, as confirmed by large clinical trials and meta-analyses. Thus, rivaroxaban possesses the most comprehensive evidence base among direct oral anticoagulants, covering the entire spectrum of clinical scenarios, from secondary prevention in isolated CAD to the management of patients with concomitant AF. This enables a truly individualized approach, carefully balancing ischemic and bleeding risks in real-world clinical practice.

By reacting pyridine or 4-(5,5-dimethyl-1,3-dioxan-2-yl)pyridine with allyl bromide, benzyl bromide and 2-(bromomethyl)-1,1-dichlorocyclopropane under heating or microwave irradiation (using a Sineo UWave-2000 microwave synthesis system with a power of 1000 W), new quaternary ammonium salts containing allyl (1-allylpyridinium and 1-allyl-4-(5,5-dimethyl-1,3-dioxan-2-yl)pyridinium bromides), benzyl (1-benzylpyridinium and 1-benzyl-4-(5,5-dimethyl-1,3-dioxan-2-yl)pyridinium bromides) or gem-dichlorocyclopropane were synthesized (1-[2,2-dichloro-1-methylcyclopropyl)methyl]pyridinium and 1-[(2,2-dichloro-1-methylcyclopropyl)methyl]-4-(5,5-dimethyl-1,3-dioxan-2-yl)pyridinium bromides) fragments. It was found that, in contrast to methyl ethyl ketone, when using acetonitrile as a solvent, the synthesis time is reduced by 2-4 times, while the yield and selectivity remain the same (≥ 95%). The best yield of salts was achieved using allyl bromide. Upon alkylation of 4-(5,5-dimethyl-1,3-dioxan-2-yl)pyridine with allyl bromide under microwave irradiation, the yield of the salt reached 80%, whereas upon interaction with 2-(bromomethyl)-1,1-dichlorocyclopropane, it decreased to 60%. Antiplatelet and anticoagulant activity was assessed for some of the obtained compounds. It was found that 1-allyl-4-(5,5-dimethyl-1,3-dioxan-2-yl)pyridinium bromide exhibited the greatest antiplatelet properties among the obtained compounds. Its activity was at the level of the reference drug, acetylsalicylic acid, but this salt increased the latent period of collagen-induced platelet aggregation (+5.7(5.2-7.3)). The anticorrosive activity of the obtained quaternary salts was determined in a model aggressive environment (GOST 9.502-82). An electrochemical method was used to study the anticorrosive activity of the substances. Electrochemical analysis was conducted on a Monicor-2M corrosion rate analyzer using two electrodes made of St3 steel. It was found that 1-allyl-4-(5,5-dimethyl-1,3-dioxan-2-yl)pyridinium bromide exhibited the highest anticorrosive activity, with a protection rate of 85% (inhibition coefficient = 6.72). For citation: Zinatullin R.R., Borisova Yu.G., Sultanova R.M., Zlotskiy S.S. Synthesis of quaternary salts of pyridine and 2-pyridine-5,5-dimethyl-1,3-dioxane and their applications. ChemChemTech [Izv. Vyssh. Uchebn. Zaved. Khim. Khim. Tekhnol.]. 2026. V. 69. N 6. P. 20-27. DOI: 10.6060/ivkkt.20266906.6817.

Characterizing Antithrombotic Regimens After Isolated Mitral Valve Repair: A Retrospective Descriptive Study and Interview of Cardiac Surgeons.

Colorectal cancer (CRC) remains one of the leading causes of cancer-related mortality worldwide, with genetic predispositions such as Familial Adenomatous Polyposis (FAP) contributing significantly to early-onset disease. This study investigated the synergic chemopreventive potential of two non-steroidal anti-inflammatory drugs (NSAIDs), acetylsalicylic acid (ASA) and sulindac (SU), in combination with a pesco-vegetarian diet (PVD), using Apc-mutated PIRC rats, a well-established model of CRC. Animals were treated over three months with two doses of ASA (800 and 1600 ppm) or a single low dose of SU (80 ppm), and tumour burden and gut microbiota composition were assessed. Results confirmed the robust protective effect of the PVD diet in reducing the intestinal tumorigenesis, particularly in the colon, independent of pharmacological treatment. ASA treatment, especially at the higher dose, significantly reduced tumour incidence in both dietary groups, with additive effects seen in combination with PVD, while SU did not show a significant protective effect. Microbiota analysis revealed distinct shifts in bacterial composition associated with both dietary and pharmacological interventions. Notably, taxa such as Roseburia and Colidextribacter, previously linked to intestinal homeostasis and anti-inflammatory activity, were modulated by ASA and diet, suggesting a microbiome-mediated chemoprevention although mechanistic effect still need to be understood. These findings underscore the independent and complementary roles of diet and pharmacological interventions in CRC prevention and highlight the gut microbiota as a promising target for future personalised preventive strategies.

Background: The dissolution of oral solid dosage forms is a key determinant of drug bioavailability, yet traditional testing methods do not capture the real-time surface dynamics of drug release. This study introduces a novel framework combining surface dissolution imaging (SDi2) with an interpretable, dual-wavelength convolutional neural network (CNN) to predict and understand dissolution behavior. Methods: Eight tablet formulations containing acetylsalicylic acid, sodium salicylate, or salicylamide, combined with either lactose or methylcellulose, were analyzed under two distinct, compendial conditions (pH 1.2 and pH 6.8). Results: Our final CNN model, which synergistically processes spectral images (280 nm for API release and 520 nm for structural changes), temporal data, and formulation composition, accurately predicted dissolution profiles, achieving a coefficient of determination of 0.89 and a root mean square error (RMSE) of 11.57. To overcome the "black-box" nature of deep learning, we employed Gradient-weighted Class Activation Mapping (Grad-CAM) to interpret the model's predictions. The analysis revealed that the model focused on tablet edges at 280 nm, consistent with surface dissolution, and on bulk regions at 520 nm, reflecting structural changes including erosion and gel-layer growth. Conclusions: These findings suggest that integrating real-time imaging with explainable AI methods can support better understanding of dissolution processes in pharmaceutical formulation development.

Multisystem inflammatory syndrome in children (MIS-C) is a severe hyperinflammatory condition that follows SARS-CoV-2 infection, characterized by persistent fever and multi-organ dysfunction. Cardiac involvement occurs in 67%-80% of cases, representing a critical clinical concern. Data from tropical and Caribbean regions remain limited in the global MIS-C literature. We conducted a cross-sectional study with retrospective data collection at Hospital Infantil Napoleón Franco Pareja, Colombia. Included patients were <18 years with a MIS-C diagnosis per WHO/CDC/RCPCH criteria and positive SARS-CoV-2 serology. Cardiac involvement was defined by elevated troponin, abnormal echocardiography, or electrocardiogram changes. Among n = 105 patients (median age 5 years, 61% male), cardiac involvement occurred in 25.7% (n = 27). The median number of affected organ systems was 4 (IQR: 3-4). Coronary artery dilation was the predominant cardiac finding (37.0% of cardiac cases), followed by mitral regurgitation and elevated troponin (both 33.3%). No patients showed left ventricular ejection fraction <55%. Treatment included corticosteroids (92.4%), acetylsalicylic acid (91.4%), and immunoglobulin (70.5%). All patients survived to discharge (100% survival). One-month follow-up revealed persistent coronary dilation in 2.9%. MIS-C affects multiple organ systems with coronary artery dilation as the predominant cardiac manifestation in our population. Favorable acute outcomes were observed with the current management protocols, including 100% survival and brief hospitalizations. However, persistent cardiac abnormalities in a subset of patients emphasize the need for systematic cardiac surveillance. These findings from a tropical Caribbean population provide insights applicable to resource-limited settings in other low- and middle-income countries.

Pharmaceutical contaminants such as aspirin (ASP), paracetamol (PAR), and ibuprofen (IBU) present increasing risks to environmental and human health, necessitating efficient detection and removal strategies. In this study, we performed a comprehensive first-principles investigation of their adsorption on a triquinoxalinylene and benzoquinone-based covalent organic framework (TQBQ-COF). The geometries were optimized and the adsorption complexes were characterized using density functional theory. The results reveal that all three drug molecules are effectively accommodated within the electron-rich central cavity of the COF, forming stable host-guest assemblies through van der Waals interactions while preserving the structural integrity of the framework. Frontier molecular orbital and global reactivity analyses indicate that drug adsorption, particularly for IBU, significantly reduces the HOMO-LUMO gap and chemical hardness, enhancing electronic sensitivity, reactivity, and charge-transfer capability. Electron density difference and non-covalent interaction analyses confirm directional electron flow from the drugs to the COF and identify stabilizing interactions governing adsorption. Simulated UV-Vis spectra show pronounced red-shifts upon drug adsorption, with the IBU@TQBQ-COF complex exhibiting the largest effect. Thermodynamic analyses further confirm spontaneous, exothermic adsorption dominated by enthalpy contributions. Collectively, these findings highlight TQBQ-COF as a highly sensitive and robust platform for drug detection and removal in aqueous and biologically relevant environments.

Acetylsalicylic acid (ASA), originally trademarked as Aspirin, is a common nonsteroidal anti-inflammatory drug (NSAID) used in human and veterinary medicine to mitigate pain and pyrexia caused by inflammatory processes. There is limited information on the effectiveness of ASA in turkey production. The objective of this study was to investigate the effect of ASA on turkey poults with induced coccidial enteritis. Two experimental trials were conducted. In both trials, the turkeys were divided into four groups: no coccidia + no ASA; no coccidia + ASA (NA); coccidia + no ASA (CN); and coccidia + ASA (CA). In both trials, turkeys in groups CN and CA were given 100× the dose of a commercial turkey coccida vaccine. Starting 48 hr postinoculation and for 7 days, the turkeys from groups NA and CA were given ASA (50 mg/kg per day). For Trial 1, ASA was given via oral gavage twice daily, whereas in Trial 2 (T2), ASA was in the drinking water. Poult weights and cloacal temperatures were recorded daily. Blood was collected daily from two randomly selected birds from each group for biochemical analysis and to assess the serum salicylic acid and nitric oxide (NO) levels. At the end of the trials, tissues were examined histologically, and immune gene expression was evaluated. Coccidia infection was the factor that had most significant influence on the majority of measured parameters. ASA had minimal to no effect on reducing clinical signs, minimizing weight loss, or controlling body temperature. These findings may be due to the rapid elimination of the drug or because sick birds did not consume sufficient ASA. In T2, it was estimated that the CA group poults consumed 31 mg/kg of ASA or less per day. Although the drinking water concentration was calculated to match the total daily intake (50 mg/kg per day), ASA's rapid metabolism meant that continuous low-level ingestion might not have reached the therapeutic plasma threshold achieved by two to three daily bolus doses. Because ASA is rapidly metabolized, a higher total daily dose may be required when provided in drinking water to maintain effective serum concentrations compared with bolus administration. Although the serum NO and tissue gene expression analysis showed that coccidia infection predominantly induces an inflammatory response, the anti-inflammatory effect of ASA administered to birds in the NA or CA groups were nil to minimal. This study highlights the complexity of ASA's effects on turkeys.