Julia Kucharczyk

Mrs. Julia Kucharczyk


Research Focus & Metrics

Academic Career Length

3Years (2024-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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Journal Article
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ADAlicja Dąbrowska
Alicja Dąbrowska
BWBartosz Wilczyński
Bartosz Wilczyński
JMJakub Andrzej Mastalerz
Jakub Andrzej Mastalerz
JKJulia Kucharczyk
Julia Kucharczyk
Julita KulbackaJulita Kulbacka
Julita Kulbacka
NRNina Rembiałkowska
Nina Rembiałkowska
Liver failure profoundly affects the immune system, leading to dysregulation of innate and adaptive immune response. This review explores the intricate relationship between liver function and immune homeostasis. The role of the liver as a central hub in immune response initiation is elucidated, emphasizing its involvement in hepatic inflammation induction and subsequent systemic inflammation. Cytokines, chemokines, growth factors, and lipid mediators orchestrate these immune processes, serving as both prognostic biomarkers and potential therapeutic targets in liver failure-associated immune dysregulation, which might result from acute-on-chronic liver failure (ACLF) and cirrhosis. Furthermore, the review delves into the mechanisms underlying immunosuppression in liver failure, encompassing alterations in innate immune cell functions such as neutrophils, macrophages, and natural killer cells (NK cells), as well as perturbations in adaptive immune responses mediated by B and T cells. Conclusion: Understanding the immunological consequences of liver failure is crucial for developing targeted therapeutic interventions and improving patient outcomes in liver disease management.

17 November 2024 in Biomedicine & Pharmacotherapy
Verified
Journal Article
Open access
NRNina Rembiałkowska
Nina Rembiałkowska
JKJulia Kucharczyk
Julia Kucharczyk
EREivina Radzevičiūtė
Eivina Radzevičiūtė
Vitalij NovickijVitalij Novickij
Vitalij Novickij
MTMargherita Tonci
Margherita Tonci
WSWojciech Kacper Szlasa
Wojciech Kacper Szlasa
Calcium electroporation (CaEP) involves the combination of calcium ions with electroporation, which is induced by pulsed electric fields (PEFs). This study explores the application of high-frequency unipolar nanosecond pulsed electric fields (nsPEFs: 8-14 kV/cm, 200 ns, 10 kHz, 100 kHz, 1 MHz repetition frequency pulse bursts, n = 100) and their potential in inhibiting lung cancer cell growth. As a reference, standard microsecond range parametric protocols were used (100 µs x 8 pulses). Methods included cell permeability quantification through Yo-Pro-1 uptake, cell viability assays, immunofluorescence studies for apoptosis and EMT markers, analysis of cell death types depending on repetition frequency pulse bursts. We determined the susceptibility of human lung cancer to electric pulses, characterized the efficacy of CaEP, and investigated cell death types depending on repetition frequency pulse bursts. We have shown that adding calcium ions to the applied nsPEF protocol increases cytotoxicity. Additionally, the use of these electroporation parameters can modulate key cellular processes, such as the epithelial-mesenchymal transition and apoptosis, as indicated by changes in the expression of markers such as E-cadherin, N-cadherin, BCL-2, and p53. Changes in cell morphology over time were observed using holotomographic microscopy. The study provides insights into the modulation of key cellular processes, indicating that nsPEF technology could improve the outcomes of conventional cancer treatments through enhanced efficacy and potentially mitigating drug resistance mechanisms. The promising results advocate for further research to optimize nsPEF protocols for clinical application, highlighting the potential of electrical fields in advancing cancer therapy.