Aspirin is used as an analgesic and antipyretic, but its release into the water bodies may also cause various diseases, such as stomach ulcers, nausea, vomiting, dizziness, and tinnitus. This study investigates the elimination of aspirin using B12N12 nanocages employing DFT simulations. Three complexes, namely, BN-Com-A, BN-Com-B, and BN-Com-C were optimized utilizing DFT-D3 correction, B3LYP theory and 6-31G(d, p) basis set. The adsorption energy values revealed strong chemisorption in BN-Com-A and BN-Com-B with Eads values greater the - 11 Kcal/mol, whereas BN-Com-C showed physisorption, having Eads values less than - 11 kcal/mol. UV-visible, IR and Raman spectra were calculated to confirm the geometry of aspirin. RDG/NCI studies were performed to verify non-covalent interactions, and QTAIM analysis was performed to determine the nature of interactions. FMO and DOS analyses showed that the HOMO-LUMO gap was reduced upon complexation. EDD and PDOS analyses explained the large orbital overlap between aspirin and the nanocage. NBO analysis showed charge transfer between the nanocage and aspirin, confirming the existence of interactions between the monomers. The PCM study shows stability of the complexes in aqueous medium depicting the effectiveness of the mechanism in aqueous medium. Recovery time calculations also demonstrated that the nanocage can be recovered and reused. Therefore, B12N12 nanocages can be considered effective in the elimination of pharmaceuticals from water and can contribute to future studies.

Low-dose aspirin is an evidence-based intervention that reduces the risk of preeclampsia and related maternal morbidity. Current U.S. guidelines recommend a risk-based approach, targeting individuals at high or moderate risk. However, implementation remains inconsistent, and risk stratification may fail to identify a substantial proportion of patients who ultimately develop preeclampsia. This paper evaluates the evidence supporting low-dose aspirin, the limitations of current risk-based strategies, and the potential benefits and harms of a universal prophylaxis approach. We argue that universal aspirin prophylaxis offers advantages in simplicity, equity, and implementation.

Thromboembolic events are an important cause of morbidity and mortality in systemic lupus erythematosus (SLE). Current thromboprophylaxis recommendations mainly focus on patients with antiphospholipid syndrome or persistent antiphospholipid antibody (aPL) positivity, whereas preventive strategies for aPL-negative patients with elevated thrombotic risk remain poorly defined. D-dimer elevation is common in SLE and has been associated with an increased risk of venous thromboembolism (VTE), but its role in guiding preventive anticoagulation remains uncertain.

Platelets are recognized as mediators of cancer progression, extending beyond hemostasis to influence tumor growth, metastatic dissemination, immune evasion, and thrombotic complications. Tumors remodel platelets through thrombocytosis and tumor cell-induced platelet aggregation, and locally through tumor-microenvironment cues that reprogram platelet function. These changes enable platelets to shield tumor cells, support epithelial-mesenchymal transition, promote angiogenesis and vascular remodeling, and establish immunosuppressive niches promoting metastasis. Platelets also drive both venous and arterial cancer-associated thrombosis via procoagulant platelet states, platelet-derived extracellular vesicles, and crosstalk with endothelium and innate immune pathways. Platelet RNA signatures and emerging proteomic/multi-omic profiling show promise for cancer detection, classification, and treatment monitoring. Preclinical and translational studies suggest that antiplatelet strategies (e.g., aspirin, P2Y12 inhibition) can modulate metastatic and thromboinflammatory pathways, motivating platelet-targeted interventions that mitigate bleeding risk. This review synthesizes platelet-tumor crosstalk linking tumor progression with cancer-associated thrombosis and vascular events and highlights emerging platelet-based biomarker and therapeutic opportunities.

Coronary artery calcium (CAC) scoring is increasingly recognised as a non-invasive tool to refine cardiovascular risk assessment, particularly in asymptomatic individuals at intermediate risk. However, its clinical use remains inconsistent, shaped by varying recommendations across international and local guidelines. This systematic review compares the major guideline documents from the Cardiac Society of Australia and New Zealand (CSANZ), the American College of Cardiology/American Heart Association (ACC/AHA) and the European Society of Cardiology (ESC), focusing on three core endpoints: eligibility criteria, therapeutic thresholds and recommendations for repeat testing. While broad agreement exists on the utility of CAC scoring in intermediate-risk populations, key differences were identified. These include divergent definitions of risk, the use of formal recommendation frameworks and inconsistencies in guidance for pharmacotherapy initiation, particularly regarding statins and aspirin. The review also highlights a lack of clarity in the role of repeat scanning and variable alignment with national risk calculators. These differences may contribute to clinical uncertainty and inconsistent implementation. In the context of rising interest in precision prevention, further research evaluating CAC-guided decision-making is needed to help eventually achieve guideline harmonisation. Clearer evidence-based guidance is needed to support equitable and effective integration into routine cardiovascular risk assessment.

Preeclampsia represents an unmasking of underlying vascular and metabolic vulnerability during the physiologic stress of pregnancy. Current first-trimester screening relies heavily on body mass index which incompletely captures qualitative metabolic dysfunction, particularly in non-obese women. In this narrative perspective, we examine the atherogenic index of plasma (AIP; log10[TG/HDL-C]), which reflects triglyceride-rich lipoprotein burden and has emerged as a marker of lipid-driven vascular stress independent of adiposity. This article does not follow systematic review methodology (e.g., PRISMA) and is intended to provide a conceptual synthesis rather than an exhaustive review. Emerging obstetric evidence suggests that first-trimester AIP (≤14 weeks) is associated with an increased risk of subsequent preeclampsia, with uric acid (UA) potentially amplifying this relationship through redox-dependent mechanisms. We propose that elevated AIP and UA define an early, detectable oxidative dyslipidemia phenotype characterized by the convergence of lipotoxic and oxidative pathways, leading to endothelial dysfunction, nitric oxide (NO) depletion, platelet activation, and impaired placental perfusion. We further delineate druggable mechanistic nodes within this axis and outline a precision pharmacology framework for biomarker-enriched prevention trials. These nodes include cyclooxygenase-1 (COX-1)-mediated platelet activation (targeted by low-dose aspirin), NO pathway dysregulation (amenable to NO-supportive strategies), and xanthine oxidase-driven oxidative amplification (a potential target of redox-modulating agents). By explicitly linking early metabolic biomarkers to defined vascular pathways, this framework reframes first-trimester screening as a platform for mechanism-guided pharmacologic investigation rather than risk categorization alone. Before clinical integration, essential steps include independent validation across diverse populations, establishment of pregnancy-specific thresholds, demonstration of incremental predictive value beyond existing screening algorithms, and evidence that biomarker-guided strategies improve maternal and perinatal outcomes. Overall, these observations should be considered hypothesis-generating and require further validation before AIP-based assessment can support biologically informed, phenotype-guided prevention strategies within obstetric pharmacology.