Antioxidant compounds such as glutathione and its enzymes have become the focus of attention of medical sciences. Glutathione, a specific tripeptide, is involved in many intercellular processes. The glutathione concentration is determined by the number of GAG repeats in gamma-glutamylcysteine synthetase. GAG polymorphisms are associated with an increased risk of schizophrenia, berylliosis, diabetes, lung cancer, and nasopharyngeal tumors. Cancer cells with high glutathione concentration are resistant to chemotherapy treatment. The oxidized form of glutathione is formed by glutathione peroxidases (GPXs). The changes in activity of GPX1, GPX2, and GPX3 isoforms may be associated with the development of cancers, for example, prostate cancer or even colon cancer. Detoxification of glutathione conjugates is possible due to activity of glutathione S-transferases (GSTs). Polymorphisms in GSTM1, GSTP1, and GSTO1 enzymes increase the risk of developing breast cancer and hepatocellular carcinoma. Gamma-glutamyl transpeptidases (GGTs) are responsible for glutathione degradation. Increased activity of GGT correlates with adverse prognosis in patients with breast cancer. Studies on genes encoding glutathione enzymes are continued in order to determine the correlation between DNA polymorphisms in cancer patients.

Introduction: The insertion (I allele) deletion (D allele) polymorphism of ACE gene (rs4646994) may influence the etiopathogenesis of multiple myeloma (MM). ACE gene is expressed in bone marrow cells and encodes angiotensin converting enzyme (ACE). It converts angiotensin I to active peptide angiotensin II, which stimulates proliferation of hematopoietic stem cells. This suggests possible association of ACE I/D gene polymorphism with MM. The aim of our study was to check possible impact of this polymorphism on risk of development and outcome of MM, as well as, sensitivity to bortezomib in cell cultures derived from MM patients. Objects and Methods: Genomic DNA from 98 newly diagnosed MM patients and 100 healthy blood donors were analyzed by PCR method. Chromosomal aberrations were detected by use of cIg-FISH. In a subgroup of 40 MM patients nucleated bone marrow cells were treated with bortezomib in vitro. Results: The Hardy-Weinberg equilibrium test showed that genotypic frequencies diverged significantly from the equilibrium. The differences between I and D allele frequencies in control and study population were significant (p=0.046). We observed the association between DD genotype and more than 2-fold risk of MM – OR=2.69; p<0.0001. We did not detect any significant differences among studied genotypes regarding clinical and laboratory parameters. Moreover we did not observe the association between survival of MM patients and I/D genotypes. Bortezomib increased number of apoptotic and necrotic cells, but the only statistically significant differences were observed in the number of viable cells at 1nM between ID and DD genotypes (p=0.026). Conclusion: Presented results confirmed the significant relationship between ACE (I/D) polymorphism and risk of MM development. We did not observe the association of ACE I/D polymorphism with disease outcome and bortezomib in vitro sensitivity.

Systemic sclerosis (SSc) is an autoimmune disorder characterized by the fibrosis of skin, heart, lung, and kidney as well. Excessive activation of fibroblasts is associated with higher expression of Notch1 and/or Notch3 genes. The constitutive expression of NOTCH genes was described in epithelial cells: epidermal keratinocytes, hair follicle cells and sebaceous glands. The NOTCH signalling pathway may be involved in the development of fibrosis, myofibroblast formation and the process of epithelial-mesenchymal transition. Activation of the NOTCH pathway leads to morphological, phenotypic and functional changes in epithelial cells. Furthermore, inhibition of Notch signalling prevent the development of fibrosis in different models, among them, bleomycin-induced fibrosis and in the Task-1 mause model. Molecular mechanisms, including the role of NOTCH signaling pathway, associated with fibrosis in SSc have not been completely recognized.

Oxidative stress and systemic inflammation are closely linked with increased risk of cancer development. Tumor necrosis factor alpha (TNF-α) is one of the pro-inflammatory cytokines. Glutathione S-transferases (GSTs) are enzymes involved in oxidative stress handling. Polymorphisms of genes encoding mentioned molecules may potentially influence the risk and the outcome in neoplastic diseases. Multiple myeloma (MM) is a haematological malignancy characterized by clonal, atypical plasma cell proliferation. In the present study we investigated the association of deletion polymorphisms in GSTT1/GSTM1 genes and single nucleotide polymorphisms (SNPs) in the TNF-α gene at positions -308/-238 with the risk and outcome in MM and sensitivity to bortezomib under in vitro conditions. One hundred newly diagnosed MM patients and 100 healthy blood donors were genotyped by means of multiplex PCR (for GSTs) and PCR-RFLP (for TNF-α). In a subgroup of 50 MM patients, bone marrow cells were treated with bortezomib in vitro. Patients with -238GA+AA or GSTT1-null genotypes had 2.0 (p=0.002) or 2.29 (p=0.013) fold increased risk of MM. The interaction effects and risk of MM were observed in GSTT1/GSTM1-null (OR=2.82, p=0.018), -308/-238GA+AA (OR=5.63, p<0.001), as well as in all combinations of -308 with GSTs. The -308/-238GA+AA genotypes in comparison to GG were associated with earlier MM onset – 61.14 vs. 66.86 years (p=0.009) and 61.72 vs. 66.52 years (p=0.035), respectively. Patients with GSTM1-present had shorter progression-free-survival (15.17 vs. 26.81 months, p=0.003) and overall-survival (22.79 vs. 34.81 months, p=0.039) compared with GSTM1-null. We did not observe relationship between response rate and studied polymorphisms. The in vitro study revealed significantly higher number of apoptotic cells at 12nM of bortezomib in GSTT1-present, GSTM1-null/present, -308GG and -238GG/GA+AA genotypes. Our findings comprise large analysis of studied polymorphisms in MM.

Persistence is defined as, among other ways, the need to achieve the goals and strive for the goal. Persistence can also be considered from the perspective of the resource concept, as a positive factor related to an individual’s adaptive behaviour, psychological resilience, and normal self-regulation. In contrast, tendencies behaviourally similar to perseverance, but which may have psychopathological features, are persistence and perfectionism. The main goal of our study was to: (I) Build non-clinical Persistence Scale (PS) in Polish and English; (II) translate in Polish and validate the Persistence, Perfectionism and Perseveration Questionnaire (PPPQ); (III) analyse properties of both scales. Methods: The study was conducted on a non-clinical group of 306 subjects. The mean age was 27.6 and ranged from 18 to 58 years. The properties of both scales were analysed using the NEO-FFI personality inventory, PSS-10 Perceived stress level scale, The UPPS-P Impulsive Behaviour Scale, the SPSRQ Sensitivity to Punishment and Reward scale, Grit scale and NAS-50 Self-Control Scale. Results: The psychometric features of the scales fulfil the requirements for psychometric tools. The factorial structure of both versions of the PS-20 scale proved to be unifactorial. Openness was the only variable to co-occur with the persistence scales of both the PS-20 and the PPPQ-10, and did not co-occur with scales intended to indicate psychopathology (Perseveration, Perfectionism). Negative correlations occurred with variables describing Persistence with levels of perceived stress, anxiety and depressive symptoms. Impulsivity measured by the SUPPS scale also showed negative correlations with the study variables. Conclusions: In the present work, we postulate that persistence is an umbrella construct that gathers and integrates many other traits to form a multi-trait persistence. Perseveration should be regarded as an undesirable trait characterising psychopathological behaviour. Desirable and indicative traits of an individual’s good functioning are persistence and, to some extent, perfectionism. Individuals with low persistence and high perseveration may be characterised by a repertoire of psychopathological behaviours.

Background/Objectives: Delirium is a common and serious neurocognitive disorder among hospitalised adults, which is associated with prolonged hospital stays, increased treatment costs, and increased mortality. Nurses, as healthcare professionals in constant contact with patients, play crucial roles in the early recognition, prevention, and management of delirium. This systematic review aimed to synthesise the evidence on nursing roles and interventions in the recognition, prevention, and treatment of delirium in hospitalised adult patients. Methods: A systematic literature search was conducted in PubMed/MEDLINE, Scopus, and CINAHL/EBSCO for studies published between January 2015 and August 2025. The protocol was registered in PROSPERO. Results: Out of the 3791 records identified, 39 met the inclusion criteria. Studies included randomised controlled trials, systematic reviews, and cross-sectional studies conducted in various hospital settings. Key nursing roles included early detection of risk factors, routine use of tools (e.g., CAM, CAM-ICU, 4AT), and implementation of multicomponent nonpharmacological prevention programs for patients with delirium. The evidence regarding the effectiveness of nurse-led interventions has been mixed: several studies reported reductions in delirium incidence and duration with early mobilisation, sleep promotion, cognitive stimulation, pain control and family involvement, whereas others reported no statistically significant effects. Conclusions: Routine screening, targeted nonpharmacological interventions, and interdisciplinary collaboration are essential for improving delirium-related outcomes. However, the findings should be interpreted with caution due to differences in the study design, variability in nursing practice across countries, and language restrictions that may have limited the scope of the review. Further high-quality studies are needed to clarify the impact of specific nursing-led strategies on delirium outcomes.