Alicja Witkowska

Liquid biopsy has emerged as one of the most promising approaches in precision oncology by enabling minimally invasive, real-time molecular characterization of tumors. Despite growing evidence, its clinical utility in urogenital cancers remains insufficiently defined. Differences in tumor biology, assay sensitivity and availability of tumor-derived material limit the assessment of its diagnostic, prognostic and predictive value across individual malignancies. This review summarizes the biological basis of liquid biopsy and evaluates its current and emerging clinical applications in prostate, bladder, renal cell, testicular, and penile cancers. Particular emphasis is placed on its potential for molecular tumor characterization, risk stratification, treatment selection, monitoring of therapeutic response and resistance, and detection of minimal residual disease. The current evidence indicates that liquid biopsy provides complementary information to tissue biopsy, particularly by enabling repeated sampling and longitudinal monitoring of tumor evolution. Its clinical value appears most relevant when tissue acquisition is challenging or dynamic molecular assessment is required. However, important limitations include low levels of tumor-derived material in selected malignancies, methodological heterogeneity, and insufficient prospective validation. Liquid biopsy should currently be considered a complementary rather than a replacement approach to tissue biopsy. Further technological advances, methodological standardization, and prospective clinical validation may facilitate its broader integration into clinical practice and support more precise diagnosis, treatment monitoring, and personalized management of urogenital cancers.

Medical errors are inevitable and will happen to almost every specialist. In anesthesiology, one of the main concerns is the inappropriate application of muscle relaxants (MRs). As this group of drugs plays a significant role in facilitating endotracheal intubation and optimizing surgical conditions, it is widely and commonly used in the medical field. To prevent residual neuromuscular block, anesthesiologists may pharmacologically reverse the neuromuscular block (NMB) by administering reversal agents. Lately, sugammadex is becoming more popular due to its ability to reverse various levels of NMB more rapidly than traditionally used acetylcholinesterase inhibitors such as neostigmine. The common challenges and errors associated with the administration of neuromuscular blocking agents (NMBAs) and muscle reversal agents include the absence of neuromuscular monitoring, underestimation of the residual block (RB), misinterpretation of DUR25, inappropriate size descriptors for muscle relaxants and reversal agents requiring weight-based dosing, the wrong dosing of rocuronium, poor usage of cisatracurium among patients with renal or hepatic failure, and the wrong usage of succinylcholine. Another source of mistakes may be inaccurate knowledge about the pharmacokinetics and pharmacodynamics of the administered drugs. Medication errors may occur not only when it comes to the usage of muscle relaxants but also with the use of reversal agents, including lack of neuromuscular monitoring, choosing the wrong antagonist strategy, “too early” administration of neostigmine, inappropriate dosing, and insufficient knowledge about drug interactions. Improving the knowledge of administered drugs and adhering to the latest recommendations could prevent many complications. This article aims to review the current challenges in the use of muscle relaxants and reversal agents in anesthesia.

Background/Objectives: Serotonin and the serotonin transporter (SERT) may have a multifaceted, but not fully understood, role in obstructive sleep apnea (OSA) and its impact on mental health in this group of patients. This study aimed to investigate changes in serotonin and the serotonin transporter (SERT) and their association with depressive and insomnia symptoms. Methods: This study included 76 participants (OSA group: n = 36, control group (CG): n = 40) who underwent polysomnography, while venous blood samples (evening and morning) were analyzed for serotonin and the SERT using ELISA. SERT mRNA expression in peripheral leukocytes was measured via quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Participants were evaluated for depression, insomnia, and quality of life (QoL). Results: This study found no significant differences in SERT mRNA or serotonin between the OSA group and CG. In the CG, individuals without mood disorders had higher baseline SERT levels and evening/morning SERT ratios than those with depression. Among the OSA participants, those with good QoL had elevated serotonin levels in the evening (p = 0.028) and morning (p = 0.043) compared to those with poor QoL. Baseline SERT protein levels were higher in the CG than in the OSA group for insomnia, while SERT mRNA expression was higher in the OSA group. Linear regression models showed 13.3% and 13.1% for non-rapid eye movement sleep (NREM) apnea/hypopnea index (AHI) and AHI variability, respectively, which was accounted for by the morning SERT level, while 30.8% of the arousal index variability was explained by the morning serotonin level. Conclusions: Serotonergic signaling may influence quality of life, depression, and insomnia in OSA, as well as the severity of the disease itself. Stratifying patients by clinical and laboratory phenotypes could enable more personalized treatment.

Hypertrophic cardiomyopathy (HCM) is a heterogeneous group of heart muscle disorders that affects millions, with an incidence from 1 in 500 to 1 in 200. Factors such as genetics, age, gender, comorbidities, and environmental factors may contribute to the course of this disease. Diagnosis of HCM has improved significantly in the past few decades from simple echocardiographic evaluations to a more complex, multimodal approach embracing advanced imaging, genetic, and biomarker studies. This review focuses on Mavacamten, a selective allosteric inhibitor of cardiac myosin, as a pharmacological treatment for HCM. Patients with HCM experience pathological actomyosin interactions, leading to impaired relaxation and increased energy expenditure. Mavacamten decreases available myosin heads, reducing actomyosin cross-bridges during systole and diastole. By reducing the number of bridges left ventricular outflow tract pressure is normalized and cardiac cavities are filled. This mechanism enhances patient performance and alleviates symptoms such as chest pain and dyspnea. The results suggest the potential for Mavacamten to transform the treatment of obstructive hypertrophic cardiomyopathy. Studies to date have shown significant improvement in exercise capacity, symptom relief, and a reduction in the need for invasive procedures such as septal myectomy. Further studies are needed to confirm the clinical results.

Obstructive Sleep Apnea (OSA) is a disorder characterized by repeated upper airway collapse during sleep, leading to apneas and/or hypopneas, with associated symptoms like intermittent hypoxia and sleep fragmentation. One of the agents contributing to OSA occurrence and development seems to be serotonin (5-HT). Currently, the research focuses on establishing and interlinking OSA pathogenesis and the severity of the disease on the molecular neurotransmitter omnipresent in the human body—serotonin, its pathway, products, receptors, drugs affecting the levels of serotonin, or genetic predisposition. The 5-HT system is associated with numerous physiological processes such as digestion, circulation, sleep, respiration, and muscle tone—all of which are considered factors promoting and influencing the course of OSA because of correlations with comorbid conditions. Comorbidities include obesity, physiological and behavioral disorders as well as cardiovascular diseases. Additionally, both serotonin imbalance and OSA are connected with psychiatric comorbidities, such as depression, anxiety, or cognitive dysfunction. Pharmacological agents that target 5-HT receptors have shown varying degrees of efficacy in reducing the Apnea-Hypopnea Index and improving OSA symptoms. The potential role of the 5-HT signaling pathway in modulating OSA provides a promising avenue for new therapeutic interventions that could accompany the primary treatment of OSA—continuous positive airway pressure. Thus, this review aims to elucidate the complex role of 5-HT and its regulatory mechanisms in OSA pathophysiology, evaluating its potential as a therapeutic target. We also summarize the relationship between 5-HT signaling and various physiological functions, as well as its correlations with comorbid conditions.

Atherosclerotic cardiovascular disease (ASCVD) stands as the leading cause of mortality worldwide. At its core lies a progressive process of atherosclerosis, influenced by multiple factors. Among them, lifestyle-related factors are highlighted, with inadequate diet being one of the foremost, alongside factors such as cigarette smoking, low physical activity, and sleep deprivation. Another substantial group of risk factors comprises comorbidities. Amongst others, conditions such as hypertension, diabetes mellitus (DM), chronic kidney disease (CKD), or familial hypercholesterolemia (FH) are included here. Extremely significant in the context of halting progression is counteracting the mentioned risk factors, including through treatment of the underlying disease. What is more, in recent years, there has been increasing attention paid to perceiving atherosclerosis as an inflammation-related disease. Consequently, efforts are directed towards exploring new anti-inflammatory medications to limit ASCVD progression. Simultaneously, research is underway to identify biomarkers capable of providing insights into the ongoing process of atherosclerotic plaque formation. The aim of this study is to provide a broader perspective on ASCVD, particularly focusing on its characteristics, traditional and novel treatment methods, and biomarkers that can facilitate its early detection.

The serotonergic pathway may impact the pathogenesis and the course of inflammatory bowel diseases (IBDs). The aim of this study was to investigate the relationship between 5-HT, the serotonin transporter (SERT), and the clinical course of the disease with the occurrence of sleep and mood disorders. Participants completed sleep questionnaires and the Beck Depression Inventory (BDI). Serum 5-HT, SERT protein expression, and mRNA levels were quantified. Additionally, patients treated with anti-TNF therapy were examined before and after treatment. In this study, 77 patients with IBD and 41 healthy controls (HCs) were enrolled and 24 of them were treated with anti-TNF therapy. Patients with IBD had higher 5-HT levels and SERT protein expression than the HCs, but not mRNA SERT levels (p = 0.015, p = 0.001, p = 0.069, respectively). Similar results were obtained for patients in the active state of the disease compared to the non-active state. There was a positive relationship between insomnia severity and SERT protein expression. BDI did not correlate with serotonin or SERT. After anti-TNF therapy, only 5-HT levels were decreased. 5-HT and SERT protein are overexpressed in active IBD and may represent a candidate for novel disease activity biomarkers. The correlation between the SERT protein level and the severity of insomnia symptoms might be among the underlying biochemical factors of sleep disturbances. Anti-TNF treatment might contribute to the reduction in 5-HT levels.