The COVID-19 pandemic has had a strong impact on people’s quality of life (QoL), which is affected by social and economic changes as well as by mental and physical health. The aim of this study was to determine QoL in post-COVID-19 patients who had required hospitalization, and to identify relevant sociodemographic data. We used questionnaires which considered demographic and socioeconomic data, health and vaccination status, the pandemic situation, and EQ-5D scoring. The interactions of all data and the scores of EQ-5D were analyzed. Multivariate logistic regression analysis was applied to the five dimensions of EQ-5D. In this single-hospital-cohort study, the average times elapsed since initial diagnosis and hospital admission were 2.5 (76.3 ± 18.1 days) and 5 months (155.4 ± 33.9 days), respectively. Post-COVID-19 females were 3–5 times more likely to be affected in terms of anxiety/depression, and in negative impact upon their usual activities, at 5 months after diagnosis. At the same time, reductions in mobility were 3–4 times more likely in elderly post-COVID-19 patients, whose levels of pain and discomfort increased. Single patients, those with low incomes, and those with severe clinical outcomes were 2–4 times more likely to experience a reduction in their usual activities, while the presence of co-morbidities and lower levels of education were associated with increased pain and discomfort. Aging-induced pain/discomfort and anxiety/depression were significantly exacerbated in elderly patients with widespread vaccination. Our study revealed effects of demographic and socioeconomic factors upon lower QoL in post-COVID-19 patients in four dimensions of EQ-5D: mobility, usual activity, pain/discomfort, and anxiety/depression, 5 months after first diagnosis and hospitalization.

Exosomes, small extracellular vesicles secreted by various cell types, have gained significant attention in cancer investigations. Isolation and characterization of exosomes derived from DOK (dysplastic oral keratinocyte), SCC (squamous cell carcinoma) and HaCaT (normal skin keratinocyte) cell lines and microRNA profiling were conducted. Magnetic sorting was applied to obtain pure exosomes. Morphology and size were characterized by transmission electron microscopy and nanoparticle tracking analysis. Validation of membrane exosomal markers (CD9, CD63) was performed via Western blotting. MiR-21, miR-31, and miR-133 levels were analyzed in exosomes and parent cells by qPCR. Biological effects of the exosomes were tested by adding them to fibroblast cultures and determining the expression of relevant carcinogenesis markers by qPCR. Exosomes appeared as cup-shaped nano-sized particles, and there was no difference regarding particle diameter and concentration between the three types of exosomes. The oncogenic miR-21 was significantly upregulated both in SCC and SCC-derived exosomes compared to DOK and HaCaT cells and their respective exosomes. However, miR-31 unexpectedly showed the highest expression in normal cells and the lowest in HaCaT exosomes. MiR-133, the tumor suppressor miRNA, was downregulated in both SCC and DOK cells compared to normal (HaCaT) cells, while the opposite situation was observed in exosomes, with HaCaT cells showing the lowest levels of miR-133. The differences in exosome content were reflected in signaling pathway activation in exosome-treated fibroblasts, with SCC exosomes exerting the most potent effect on several cancer-related pathways, notably PIK3/AKT, PTEN, and NOTCH signaling cascades.

Cancer-promoting proinflammatory microenvironment influences colorectal cancer (CRC) development. We examined the biomarkers of inflammation, intestinal differentiation, and DNA activity correlated with the clinical parameters to observe progression and prognosis in the adenocarcinoma subtype of CRC. Their immunohistology, immunoblotting, and RT-PCR analyses were performed in the adenocarcinoma and neighboring healthy tissues of 64 patients with CRC after routine colorectal surgery. Proinflammatory nuclear factor kappa B (NFκB) signaling as well as interleukin 6 (IL-6) and S100 protein levels were upregulated in adenocarcinoma compared with nearby healthy colon tissue. In contrast to nitrotyrosine expression, the oxidative stress marker 8-Hydroxy-2′-deoxyguanosine (8-OHdG) was increased in adenocarcinoma tissue. Biomarkers of intestinal differentiation β-catenin and mucin 2 (MUC2) were inversely regulated, with the former upregulated in adenocarcinoma tissue and positively correlated with tumor marker CA19-9. Downregulation of MUC2 expression correlated with the increased 2-year survival rate of patients with CRC. Proliferation-related mammalian target of rapamycin (mTOR) signaling was activated, and Ki67 frequency was three-fold augmented in positive correlation with metastasis and cancer stage, respectively. Conclusion: We demonstrated a parallel induction of oxidative stress and inflammation biomarkers in adenocarcinoma tissue that was not reflected in the neighboring healthy colon tissue of CRC. The expansiveness of colorectal adenocarcinoma was confirmed by irregular intestinal differentiation and elevated proliferation biomarkers, predominantly Ki67. The origin of the linked inflammatory factors was in adenocarcinoma tissue, with an accompanying systemic immune response.

Thrombosis is a critical complication in lymphomas, driven by chronic inflammation. To observe this systemic mechanism, we evaluated inflammatory cytokines, neutrophil and monocyte activation, and platelet function in diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), and Hodgkin lymphoma (HL), with and without thrombosis using ELISA and flow cytometry according to laboratory and clinical data. Interleukin-1β was elevated across lymphomas and inversely correlated with the Khorana score for venous thromboembolism, while increased tumor necrosis factor-alpha (TNF-α) was inversely associated with the International Prognostic Index (IPI) in thrombosis-associated lymphomas. Neutrophil activation was increased in DLBCL, while elevated neutrophil extracellular traps (NETs) biomarkers were inversely consistent with thrombosis and the ThroLy score. NETs were elevated in HL. Classical monocytes were increased in all lymphoma subtypes, with intermediate and tissue factor (TF)-carrying monocytes elevated in DLBCL and HL. Platelet activation was pronounced, with platelet–monocyte aggregates and platelet-associated TF elevated in DLBCL and FL but not HL. P-selectin was increased in lymphomas with thrombosis, aligned with Khorana and ThroLy scores, and reflected clinical stage while inversely correlating with IPI in non-thrombotic lymphomas. These findings highlight distinct thromboinflammatory mechanisms across lymphoma subtypes, providing insights into biomarkers for thrombosis risk and therapeutic targets in lymphoma management.

The severity and mortality of coronavirus disease 2019 (COVID-19) are greater in males than in females, though the infection rate is the same in the two sexes. We investigated sex hormone differences associated with the hyperinflammatory immune response to SARS-CoV-2 on the basis of patients’ cytokine profiles and vaccination statuses. Clinical and laboratory data of 117 patients with COVID-19 were collected to examine sex differences associated with oxidative stress markers, neutrophil extracellular traps (NETs), and plasma cytokine levels up to 5 months from hospital admission. The testosterone and free testosterone levels were low in male patients with COVID-19 and returned to normal values after recovery from the disease. The dihydrotestosterone (DHT) levels were transiently reduced, while the sex hormone-binding globulin levels were decreased in post-COVID-19 male patients. The levels of the inflammatory cytokines interleukin-6 (IL-6) and IL-10 appeared generally increased at diagnosis and decreased in post-COVID-19 patients. In females, the concentration of tumor necrosis factor-alpha was increased by four times at diagnosis. The levels of the coagulation markers intercellular adhesion molecule-1 (ICAM-1) and E-selectin were consistently upregulated in post-COVID-19 female patients, in contrast to those of vascular cell adhesion molecule-1 (VCAM-1), P-selectin, and chemokine IL-8. DHT increased the levels of reactive oxygen species in the neutrophils of male patients, while estradiol decreased them in females. Markers for NET, such as circulating DNA and myeloperoxidase, were significantly more abundant in the patients’ plasma. Sex hormones have a potential protective role during SARS-CoV-2 infection, which is weakened by impaired testosterone synthesis in men.

Two new Ru(II) complexes, mononuclear [RuCl₂(η⁶-p-cymene)(3,4-dmph-κN)] (1) and the binuclear complex [{RuCl(η⁶-p-cymene)}₂(μ-Cl)(μ-3,4-dmph-κ²N,N′)]Cl (2; 3,4-dmph = 3,4-dimethylphenylhydrazine), are synthesized and experimentally and theoretically structurally characterized utilizing ¹H and ¹³C NMR and FTIR spectroscopy, as well as DFT calculations. Degradation product of 2, thus ([{RuCl(η⁶-p-cymene)}₂(μ-Cl)(μ-3,4-dmph-κ²N,N′)][RuCl₃(η⁶-p-cymene)] (2b) was characterized with SC-XRD. In the crystals of 2b, the cationic and anionic parts interact through N-H^...Cl hydrogen bridges. The spectrofluorimetric measurements proved the spontaneity of the binding processes of both complexes and HSA. Spin probing EPR measurements implied that 1 and 2 decreased the amount of bound 16-doxylstearate and implicated their potential to bind to HSA more strongly than the spin probe. The cytotoxicity assessment of both complexes against the MDA-MB-231 and MIA PaCa-2 cancer cell lines demonstrated a clear dose-dependent decrease in cell viability and no effect on healthy HS-5 cells. Determination of the malondialdehyde and protein carbonyl concentrations indicated that new complexes could offer protective antioxidant benefits in specific cancer contexts. Gel electrophoresis measurements showed the reduction in MMP9 activity and indicated the potential of 1 in limiting the cancer cells’ invasion. The annexin V/PI apoptotic assay results showed that 1 and 2 exhibit different selectivity towards MIA PaCa-2 and MDA-MB-231 cancer cells. A comparative molecular docking analysis of protein binding, specifically targeting acetylcholinesterase (ACHE), matrix metalloproteinase-9 (MMP-9), and human serum albumin (HSA), demonstrated distinct binding interactions for each complex.