Diabetic foot ulcers (DFUs) are chronic, infection-prone wounds that heal poorly due to impaired angiogenesis, persistent inflammation, and elevated oxidative stress, creating a substantial clinical and economic burden and highlighting the need for advanced extracellular matrix-mimicking dressings. Therefore, we have developed a ferulic acid (FA)-esmolol (ESM)-loaded coaxial nanofibrous (NFs) scaffold using silk sericin (SS) as the shell and poly(lactic acid) (PLA) as the core via electrospinning for DFU management. The optimized scaffold showed a uniform, bead-free morphology with increased fiber diameter (370 ± 95 nm) compared to blank NFs (201 ± 52 nm) and a confirmed core-shell architecture. The FA-ESM NFs demonstrated high porosity (81.04 ± 4.39%) and an optimal water vapor transmission rate (WVTR) (2077 g/m[2]/day), supporting a moist wound environment. Water retention (409.39 ± 12.41%) and controlled biodegradation (~98% over 21 days) indicated excellent exudate handling and sustained structural integrity. Mechanical analysis showed suitable tensile strength (1.20 MPa) and elongation (112.80%). Drug release followed the Korsmeyer-Peppas model (R[2] ≈ 0.975/0.9811; n = 0.699/0.883), indicating anomalous to case II transport. The scaffold exhibited significant antioxidant activity, >80% cell viability, and hemocompatibility. It significantly enhanced cell migration within 48 h and modulated biomarkers (↓MMP-9, ↓TNF-α, ↑VEGF; p < 0.01). Strong antibacterial activity against Staphylococcus aureus and Pseudomonas aeruginosa, along with significantly accelerated wound closure in diabetic models within 16 days (p < 0.0001), further validates its therapeutic efficacy. Overall, the scaffold demonstrates promising anti-inflammatory, antioxidant, and pro-angiogenic properties and potentially effective dressing for DFU management.

Beta-blockers are among the most widely prescribed drugs in the management of both supraventricular and ventricular arrhythmias, and they are frequently regarded as a homogeneous pharmacological class. They are not. The agents in current use differ substantially in beta1-receptor selectivity, lipophilicity, half-life, route of administration, intrinsic sympathomimetic activity, and ancillary properties, and arrhythmias themselves differ in mechanism, adrenergic dependence, anatomical origin, and structural substrate. This narrative review examines whether these pharmacological differences translate into clinically meaningful differences in efficacy and utility, asking not only whether a beta-blocker should be used but which one should be used. Evidence was drawn from a targeted search of PubMed, Web of Science, Scopus, Ovid, Embase, and the Cochrane Library, with priority given to randomized controlled trials, meta-analyses, large registries, and contemporary society guidelines, and was synthesized qualitatively by arrhythmia type. A class effect is apparent for many indications, particularly rate control in atrial fibrillation and atrial flutter, where metoprolol, bisoprolol, and carvedilol perform broadly similarly and the choice is driven mainly by comorbidity and tolerability. Drug-specific differences emerge in three settings. In adrenergically mediated inherited syndromes, namely catecholaminergic polymorphic ventricular tachycardia and long QT syndrome, nonselective agents and especially nadolol are clearly superior to beta1-selective agents, and the same principle appears to extend to ventricular electrical storm, in which propranolol has outperformed metoprolol in a randomized comparison. In acute care, pharmacokinetics dominate, and the ultra-short-acting agents esmolol and landiolol permit a degree of titration that longer-acting drugs cannot match. In patients with heart failure and reduced ejection fraction, carvedilol, metoprolol succinate, and bisoprolol should be preferred irrespective of arrhythmia subtype because of their established mortality benefit. Conversely, beta1-selective agents, including the highly selective agent nebivolol, improve tolerability in bronchospastic disease, although this reflects respiratory tolerability rather than any demonstrated antiarrhythmic advantage, and beta-blockers have little role in Brugada syndrome or in bradycardia-dependent acquired torsades de pointes. Beta-blockers should therefore not be treated as interchangeable. Selection should integrate arrhythmic mechanism, structural substrate, and patient characteristics, and head-to-head trials remain conspicuously scarce.

Awake craniotomy is a standard neurosurgical technique that enables real-time assessment of brain functions during tumor resection, with high success rates. Although highly effective, the procedure is associated with hemodynamic disturbances, including blood pressure variability and impaired cerebral perfusion, compromising intraoperative safety. A focused literature search of PubMed, Embase, and Google Scholar was performed to identify relevant studies on intraoperative hemodynamic management during awake craniotomy. Findings were synthesized narratively to summarize current evidence, highlight emerging strategies, and identify knowledge gaps. Hypertension (8%-34%) was the most common disturbance, often triggered by painful surgical stimuli or emergence from sedation, with repeat craniotomy, impaired autoregulation, and glioma pathology as additional risk factors. Hypotension (10%-11%) was linked to perioperative stroke and mortality. Cerebral hypoperfusion contributed to poor outcomes, with stroke up to 23% and neurological morbidity in 68% of patients. Preventive strategies, such as scalp blocks, individualized blood pressure targets, and the use of dexmedetomidine and midazolam, improved intraoperative stability, while short-acting agents, including esmolol and labetalol, were preferred for rapid control. Advanced monitoring modalities, including arterial lines, near-infrared spectroscopy, and cerebral autoregulation indices, enhance safety and support accurate functional mapping. Hemodynamic instability during awake craniotomy influences outcomes. Current evidence supports multimodal prevention, tailored blood pressure control, and short-acting pharmacological agents; practice variation and the lack of randomized trials limit standardization. Looking ahead, advanced monitoring and emerging AI systems may provide new opportunities to enhance cerebral protection and optimize patient safety. This review summarizes evidence on intraoperative hemodynamic control in awake craniotomy, emphasizing strategies that enable maximal safe resection while preserving neurological function.

Background: Our research group has previously demonstrated the protective effect of short-term treatment with esmolol on large artery remodeling. However, whether this beneficial effect persists after treatment withdrawal remains unknown. Therefore, the aim of the present study was to investigate whether regression of thoracic aorta remodeling after a short-term esmolol treatment persists following drug withdrawal. Methods: Adult male spontaneously hypertensive rats (SHRs) received either esmolol (300 µg/kg/min) or vehicle (saline solution) by continuous infusion for 48 h. Following treatment, animals were evaluated either immediately (SHR-E 48 h group) or after withdrawal periods of 7 days (SHR-E 7 d group) or 1 month (SHR-E 1 m group). Hemodynamic parameters, thoracic aorta geometry, extracellular matrix composition (elastin and collagen), and the passive mechanical response of the arterial wall (β parameter) were assessed in all animals. Results: Forty-eight hours of esmolol treatment significantly reduced blood pressure and attenuated thoracic aortic wall thickness, external diameter, cross-sectional area, collagen content and elastic fiber density. Additionally, passive mechanical testing showed a significant reduction in the β parameter, indicating improved arterial compliance after treatment. Remarkably, these structural and mechanical benefits persisted for up to one month after withdrawal, despite the return of blood pressure to hypertensive levels. Conclusions: Protective effect of esmolol on aortic remodeling is persistent after treatment withdrawal in SHRs, perhaps independent of blood pressure.