Background: Cytokine storm is a life-threatening immune reaction contributing to the severity of various infectious diseases such as COVID-19, sepsis, Ebola, and Dengue. Understanding its pathophysiology is critical for timely diagnosis and effective treatment. Methods: A narrative review was conducted using PubMed, Scopus, and Web of Science (September 2024 – January 2025). Keywords included “cytokine storm,” “pro-inflammatory cytokines,” “COVID-19,” “sepsis,” “targeted therapy,” and “personalised medicine.” Studies were analysed thematically. As a narrative review, the findings are limited by the heterogeneity and potential bias of included studies, and no quantitative synthesis was performed. Results: The review outlines key mechanisms of cytokine storm, such as IL-6, IL-10, and TNF-α overproduction, and presents clinical cutoff values (e.g., IL-6 > 19.5 pg/mL) associated with disease severity. Targeted therapies (e.g., tocilizumab, anakinra), immunomodulators (e.g., JAK inhibitors), stem cell therapy, and plasmapheresis were reviewed. A personalised approach to treatment based on biomarkers and comorbidities was emphasised. Conclusions: Cytokine storm remains a major challenge in infectious disease management. While therapeutic strategies are evolving, individualised, biomarker-driven treatment offers the greatest potential for improving outcomes

Organ transplantation offers unique opportunities to patients with advanced organ diseases. These opportunities include the significantly improved survival and quality of life. Two examples may be given to demonstrate the gains.

The first scenario is heart failure. The expected life span of an individual with advanced heart failure may be as short as twelve to twenty months. If compared to the average survival of more than ten years after the heart transplantation (1), the benefits of this operation appear self-explanatory. The second example is renal failure. A typical patient with chronic kidney failure must undergo three dialysis sessions per week. However, in the modern era, the projected median graft survival for the deceased donors is above 11 years, and for living donors, it is above 19 years, granting freedom from dialysis for this time (2).

The improvements in longevity and quality of life after organ transplantation are jeopardized by a number of reasons. To name the most common, those are graft rejections and numerous side effects of immunosuppression. Graft rejections ultimately lead to the organ failure, while immunosuppressants place the patients at risk of infections, cardiovascular disorders, and cancer. Sophisticated postoperative follow-up protocols have been introduced to address the hazards. Among many activities, they include regular interventions aiming at the early detection of rejections and malignancies.

In this issue of Heart Vessels and Transplantation, Mohamed MSA brought attention to angiogenesis in various scenarios, including the recipients after organ transplantations (3). The author suggested angiogenesis monitoring could be helpful both in the early and late postoperative periods as a part of follow-up screening.

Progressive angiogenesis in the implanted graft shortly after transplantation promotes postischemic recovery and maintains normal organ function. Therefore, diminished angiogenesis activity could serve as an early marker of graft failure. This pathophysiological axis is evidently most crucial in the first weeks to months postoperatively. Although the message appears clear, when trying to address it in practice, numerous obstacles must be kept in mind. For instance, some traditional markers of angiogenesis, such as vascular endothelial growth factor (VEGF) are actually proinflammatory, overlapping with rejection. In other words, interpretation of isolated VEGF levels may be misleading.

Conversely, persisting high angiogenesis activity in the long term after transplantation may suggest the development of cancer. This aspect should draw attention beginning from the second post-transplantation year. Again, practical assessment may be not straightforward. For instance, elevated VEGF blood level after cardiac transplantation is a strong marker of chronic coronary vasculopathy, which means the specificity of this marker for malignancy in the cardiac recipients will be low.

In the view of the existing challenges of practical assessment of angiogenesis activity via blood-based assays, Mohamed MSA (3) conducted a narrative search to identify its markers and performed in vitro experiments on cell lines.

The investigator concluded that four mediators need to be checked to assess the angiogenetic profile: VEGF, endothelin-1, nitric oxide synthase trafficking inducer (Nostrin), and endothelial nitric oxide synthase (eNOS). With this approach, both the pro- and anti-angiogenic sides of the continuum would be taken into account with potentially robust conclusions.

Clinical studies need to demonstrate if the suggested approach in post-transplantation patients can help in the detection of unwanted early and late pathophysiological patterns.

In 2023, two Correspondence published in The Lancet Infectious Diseases highlighted the growing apprehension regarding extensively drug-resistant bacteria originating from Ukraine, exacerbated by the ongoing conflict.1,2 However, there is a paucity of large granular and localised datasets to substantiate and guide international response efforts.
We report on this crucial gap by presenting findings from over 6800 diagnostic isolates obtained from the largest health-care union in Western Ukraine collated as part of development of a yearly cumulative antibiogram (CuAbgm) to track antibiotic-resistant bacteria in our region; the study period took place between May 1, 2023, and April 30, 2024. Hospitals within the First Lviv Territorial Medical Union (1TMO) contain over 2400 beds and provide treatment for more than 100 000 patients annually. 1TMO is an essential hospital union in the trauma evacuation pathway, receiving war-wounded casualties for definitive reconstruction surgery and burns treatment from other Ukrainian hospitals.

   Upconverting nanoparticles (UCNPs) have attracted much attention in nanomedicine due to their ability to upconvert photons. However, their adverse effects hinder the biomedical applications. In this paper, bisphosphonate-modified poly(isobutylene-alt-maleicacid)-graft-poly(N,N-dimethylacrylamide)-coated NaYF4:Yb,Er,Pr UCNPs (UCNP@PIMAPDMA) nanoparticles were designed, which exhibited luminescence emission simultaneously in the visible and NIR-II regions. The developed UCNPs were characterized by a range of physicochemical methods, including transmission electron and energy dispersive microscopy (TEM and EDAX), dynamic light scattering (DLS), X-ray diffraction analysis (XRD), spectrofluorometry, X-ray photoelectron spectroscopy (XPS), and so forth. The UCNP@PIMAPDMA nanoparticles were also evaluated in cell cultures and experimental animals. The particles showed good biocompatibility with cultured human embryonic kidney HEK293 cells commonly used in toxicological studies. Neat UCNPs were cytotoxic towards these cells, which was confirmed by measuring their viability using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric assay. Blood serum proteins adhered to the surface of UCNP@PIMAPDMA particles, forming a protein corona that may contribute to particle biosafety. After intravenous injection of these particles into laboratory mice, there were no statistically significant changes in body mass of the treated animals. Also, no big adverse effects on blood cell profile, enzymatic and metabolic markers of hepatotoxicity and nephrotoxicity were observed. Finally, the application potential of UCNP@PIMAPDMA nanoparticles was confirmed by successfully imaging the cytoplasm of rat mesenchymal stem cells and rat C6 glioblastoma cells using laser scanning confocal microscopy.

Keywords: cytotoxicity | hematology parameters | polymer coating | protein corona | upconverting nanoparticles

UDC: 616.94:576.8.06:616.155.34:616.155.321]-002.828-092.9

   Background. Sepsis is a major global health problem, with fungal pathogens such as Candida albicans emerging as a significant cause of invasive infection. Fungal sepsis has a higher mortality rate than bacterial sepsis and is complicated by antifungal resistance. Although neutrophil extracellular traps (NETs) help to contain fungi, excessive NETs can contribute to inflammation and tissue injury. Understanding these mechanisms could reveal markers of disease activity and new therapeutic targets. Materials and Methods. Fungal sepsis was induced in twelve male BALB/c mice via an intraperitoneal injection of Meyerozyma guilliermondii (107 cells per mouse). Blood was collected at the beginning of the study and then on days 1–3, 7–9, and 13–15. Serum was analyzed for IgG, IgM, circulating immune complexes (ELISA), and extracellular DNA (fluorescence assay). 
   Results and Discussion. In mice with fungal sepsis, IgG levels remained stable while IgM levels increased significantly between days 7 and 9, before declining from day 13. IgG–IgM immune complexes peaked around days 8–9, reflecting active antigenantibody responses. Free DNA levels, which indicate NETs formation, increased by day 7 and then declined, showing early neutrophil activation followed by humoral control. Together, these findings suggest a coordinated immune response in which NETs and immune complexes contribute to both pathogen control and inflammation.
   Conclusion. Fungal sepsis induced by Meyerozyma guilliermondii resulted in early NETosis and an increase in IgM and immune complexes. IgM levels peaked on days 7–9 before declining. Unlike Candida albicans, this strain does not cause rapid lethality, enabling detailed tracking of disease progression over time. After day 9, immune parameters began to normalize, indicating the resolution of the acute phase and supporting the usefulness of this model for studying host immune dynamics in fungal sepsis.
   Keywords: fungal sepsis, Meyerozyma guilliermondii, acute inflammation, immune defense, circulating immune complexes, neutrophil extracellular traps
(NETs)