The Medical University of Łódź was founded on October 1, 2002 as a merger of the Medical Academy of Łódź (founded January 1, 1950) and the Military Medical Academy of Łódź (founded July 1, 1958). It is the largest teaching hospital unit in Poland and a European research center.
Background: Severe asthma affects approximately 5–10% of the asthma population and is characterized by significant heterogeneity in pathophysiology and clinical presentation. The condition is traditionally categorized into Type 2-high (T2-high) inflammation, driven by mechanisms such as eosinophilia and IgE mediation, and Type 2-low (T2-low) inflammation, which is less well-defined. Standard treatments involving broad immunosuppression with corticosteroids are often insufficient or associated with toxicity in severe cases. Consequently, the understanding of asthma has evolved from a "one-size-fits-all" approach to a precision medicine model based on specific phenotypes and endotypes. Aim: The aim of this review is to examine the efficacy, safety, and selection of biological therapies for severe asthma. Materials and Methods: The review included scientific papers sourced from the PubMed and Google Scholar databases. Results: Monoclonal antibodies have transformed severe asthma management. Omalizumab addresses allergic asthma, while anti-IL-5 agents (mepolizumab, reslizumab, benralizumab) effectively reduce exacerbations in eosinophilic phenotypes. Dupilumab (targeting IL-4/IL-13) offers superior lung function improvement, particularly in mixed phenotypes. Notably, tezepelumab (anti-TSLP) and emerging anti-IL-33 agents demonstrate efficacy across a broader spectrum, offering new therapeutic options for previously refractory T2-low patients. Conclusions: Biologics have shifted the therapeutic goal from disease control to clinical remission. While T2-high asthma is well-managed by existing targeted therapies, upstream inhibitors now provide vital solutions for the challenging T2-low population. Consequently, a precise, biomarker-driven approach is essential to select the optimal therapy and maximize patient outcomes.
BACKGROUND The Dark Triad Scale (DTS) encompasses 3 personality traits: narcissism, psychopathy, and Machiavellianism. While numerous studies have explored the structure and social, medical, and behavioral implications of Dark Triad personality, its association with attitudes toward brain death, organ donation, and futile therapy has not been previously examined. The aim of this study was to assess how DTS traits influence perceptions of these end-of-life issues. MATERIAL AND METHODS This cross-sectional study used the DTS and an original questionnaire. Participants included Polish paramedic and midwifery students (n=48) and non-medically educated (NM) individuals recruited via Facebook (n=88). Due to underrepresentation of males in the NM group, only female respondents (n=75) from this group were included in cluster analysis. RESULTS Students of both genders were significantly more willing to become organ donors after death than were NM participants (mean score 3.92±1.3 vs 3.33±1.4 on a 1-5 scale; P=0.014). Among male and female students, higher Machiavellianism was associated with the belief that futile therapy is unethical. In NM females, psychopathy was correlated with denial of the existence of brain death, while Machiavellianism correlated with acceptance of withdrawing futile therapy. Cluster analysis identified 3 subgroups of NM females. Individuals with the highest levels of Dark Triad traits showed the greatest acceptance of withdrawing futile therapy, whereas those tending to deny brain death had moderate levels of these traits. CONCLUSIONS DTS traits are associated with attitudes toward futile therapy and brain death. Higher Machiavellianism is linked to greater acceptance of withdrawing futile therapy, while denial of brain death among females is associated with intermediate Dark Triad traits and higher psychopathy.
Hormonal regulation is essential for maintaining physiological homeostasis and enabling adaptation to physical stress, making the endocrine system a key factor influencing athletic performance and training responses. Hormones such as thyroid hormones, cortisol, testosterone, and growth hormone regulate metabolism, cardiovascular function, muscle performance, and recovery. Disruptions in endocrine function—resulting from gland disorders or training-related factors such as low energy availability—may impair exercise capacity and adaptation to training. This narrative review summarizes recent literature on the relationship between selected endocrine disorders and sports performance, focusing on thyroid dysfunction, cortisol-related disorders, and pituitary abnormalities. Evidence suggests that thyroid disorders can affect cardiovascular efficiency, neuromuscular performance, and metabolism, while adrenal dysfunction may impair stress responses and exercise tolerance. Hypercortisolism and Cushing syndrome are associated with reduced aerobic capacity, muscle weakness, and sarcopenia, whereas pituitary dysfunction, including that related to traumatic brain injury or relative energy deficiency in sport, can disrupt multiple hormonal axes and influence physical capacity. Overall, endocrine disorders may significantly affect physical performance and athlete health. Early detection, regular hormonal monitoring, and individualized medical and training strategies are essential to support safe training and optimize performance outcomes.
The posterior interosseous ligament (PIL) of the ankle syndesmosis remains a poorly recognized and inconsistently described structure, despite growing anatomical and biomechanical evidence supporting its relevance. Historically conflated with the deep component of the posterior inferior tibiofibular ligament (PITFL), the PIL has only recently gained attention as a potentially independent contributor to syndesmotic stability. This review consolidates current anatomical, biomechanical, radiological, and surgical insights into the PIL, clarifies terminological inconsistencies, and evaluates its clinical significance. A comprehensive synthesis of cadaveric studies, imaging research, and biomechanical models was undertaken to characterize the morphology, function, detectability, and surgical relevance of the PIL. The PIL is identifiable in up to 80
Background:Clinical trial designs evaluating on-demand therapies for hereditary angioedema attacks have evolved in response to changes in treatment guidelines. Sebetralstat, an oral plasma kallikrein inhibitor, was evaluated in 2 randomized, placebo-controlled clinical trials, which instructed early treatment of attacks with no minimum severity requirement. Objective:Characterize the efficacy and safety of sebetralstat by pooling data from phase 2 and 3 trials. Methods:This pooled analysis included participants (phase 2, aged ≥18 years; phase 3, aged ≥12 years) who received ≥1 dose of study drug (phase 2, sebetralstat 600 mg or placebo; phase 3, sebetralstat 300 mg or 600 mg, or placebo). Efficacy outcomes included times to beginning of symptom relief within 12 h, reduction in severity within 12 h, and complete attack resolution within 24 h. P values were not adjusted for multiplicity. Results:377 attacks were treated: 87 with sebetralstat 300 mg; 151 with sebetralstat 600 mg; 139 with placebo. Median (interquartile range) time to treatment was 32.5 min (8.0-94.0). Baseline severity was rated as "Mild" (46.2%), "Moderate" (40.6%), or "Severe"/"Very Severe" (12.7%). Compared with placebo, time to beginning of symptom relief was faster with sebetralstat (300 mg; 600 mg [P = 0.0001; P < 0.0001]), as was reduction in severity (P = 0.0038; P < 0.0001) and complete attack resolution (P = 0.0021; P < 0.0001). Median time to beginning of symptom relief was 1.6 h (0.8-7.0) and 1.8 h (1.0-4.3) with sebetralstat 300 mg and 600 mg, respectively, and 8.3 h (1.5 to >12) with placebo. Sebetralstat had a safety profile comparable to placebo. Conclusion:Across phase 2 and 3 clinical trials, sebetralstat enabled early treatment, provided effective symptom relief versus placebo, and was well tolerated, regardless of attack location or baseline severity. Clinical trial registration:ClinicalTrials.gov Identifier NCT04208412, registered on 2019-07-02; ClinicalTrials.gov Identifier NCT05259917 (KONFIDENT), registered on 2022-02-22.
