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    Medical University of Lodz

    院校EST. 2002
    1.8万论文总数
    39万引用总数

    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.

    论文量&引用量时间轴

    机构学者

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    Maciej Banach
    Maciej Banach
    Department of Preventive Cardiology and Lipidology, Medical University in Lodz;Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine;Liverpool Centre for Cardiovascular Science, The University of Liverpool
    论文:743引用:0H-index:0
    Tadeusz Robak
    Tadeusz Robak
    Department of Hematology, Medical University of Lodz
    论文:634引用:0H-index:0
    Wojciech Mlynarski
    Wojciech Mlynarski
    Department of Pediatrics, Oncology, Hematology and Diabetology, Medical University of Lodz
    论文:397引用:0H-index:0
    Janusz Szemraj
    Janusz Szemraj
    Department of Medical Biochemistry, Medical University of Łódź
    论文:336引用:0H-index:0
    Piotr Kuna
    Piotr Kuna
    Klinika Chorob Wewnetrznych, Astmy i Alergii, Medical University of Łodz
    论文:311引用:0H-index:0
    Wojciech Fendler
    Wojciech Fendler
    Department of Pediatrics, Medical University of Lodz
    论文:295引用:0H-index:0
    Jakub Fichna
    Jakub Fichna
    Dept Biochem, Med Univ Lodz
    论文:294引用:0H-index:0
    Jacek Rysz
    Jacek Rysz
    Department of Nephrology, Hypertension and Family Medicine, Medical University of Lodz
    论文:288引用:0H-index:0
    Marek L. Kowalski
    Marek L. Kowalski
    Department of Immunology and Allergy, Medical University of Lodz
    论文:255引用:0H-index:0

    论文(10000)

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    1MicroRNAs As Current Diagnostic Biomarkers and Potential Therapeutic Targets in Allergic and Non-Allergic Rhinitis – A Functional Characterization
    Dominik Przychodniak, Wojciech Michał Jankowski,Marcin Kurowski

    Allergic rhinitis affects up to one-quarter of the population in industrialized countries. This chronic inflammatory disease of the nasal mucosa is triggered by allergen exposure and mediated by immunoglobulin E, leading to immune dysregulation. Diagnosis typically relies upon skin prick tests, serum-specific immunoglobulin E levels and nasal allergen provocations. Differentiation from non-allergic rhinitis remains a diagnostic challenge. Recent research has identified novel microRNAs, small non-coding RNA regulating post-transcriptional gene expression, as key regulators of immunological pathways with great potential as disease-specific targets in diagnostics and therapy. The purpose of this review is to explore novel therapeutic and diagnostic possibilities regarding novel miRNAs. This functional review evaluated current evidence specific to miRNA expression in allergic and non-allergic rhinitis. Seven microRNAs (miR-29a, miR-135a, miR-143, miR-146a, miR-150-5p, miR-223, miR-451) are discussed as potential diagnostic markers and therapeutic agents in the future. Interventional studies, including human and animal studies, are reviewed. The available evidence suggested that selected microRNAs may show specificity and sensitivity as biomarkers for allergic and non-allergic rhinitis in future human trials. Therapeutic options involving miRNAs have shown great promise but still lack validation in clinical studies. In this review, we have identified several challenges in microRNA-based diagnostic approaches and suggested strategies to facilitate future development. MiRNA research in AR has revealed their role as both diagnostic biomarkers and therapeutic agents in several different mechanisms that are currently under investigation. Dysregulation of miRNA expression has been documented in asthma and allergic rhinitis, but data regarding non-allergic rhinitis remain limited.

    2026Current Allergy and Asthma Reports(2026)引用:81
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    2GLP1-E2 Therapy Delays Autoimmune Diabetes in Late-Stage Prediabetic NOD Mice and Potentiates Low-Dose Anti-Cd3 Therapy for Enhanced Disease Protection
    Laure Degroote,Jędrzej Chrzanowski, Pierre Lemaitre, Amber Wouters, Stephanie Bourgeois, Annelore Van Mulders, Julie Pierreux, Sophie Coenen, Lien Willems,Gunter Leuckx, Marijke Viaene, Marc Packbier,

    Anti-CD3 monoclonal antibody (aCD3) delays progression to stage 3 type 1 diabetes in high-risk individuals by modulating autoimmune activity. Nevertheless, responses remain variable and transient, with therapy providing only indirect beta cell protection. We investigated whether glucagon-like peptide-1–17ß-oestradiol conjugate (GLP1-E2), a beta cell-targeted fusion compound that enhances beta cell survival and function, could potentiate a short low-dose aCD3 course in preventing autoimmune diabetes in NOD mice. We hypothesised that co-targeting immune dysregulation and beta cell fragility would provide complementary and potentially synergistic benefits, resulting in more durable protection than either monotherapy. Female late-stage prediabetic NOD mice were randomised into four groups: untreated controls, aCD3 monotherapy, GLP1-E2 monotherapy and combination therapy. aCD3 was administered intravenously at 2.5 µg/day for 5 consecutive days, while GLP1-E2 was given subcutaneously at 100 nmol kg−1 day−1 for 18 weeks. Mice were monitored longitudinally for diabetes onset. The pancreas was analysed by spatial transcriptomics and immunostaining to assess immune infiltration, beta cell integrity and molecular pathway alterations. At 30 weeks of age, diabetes incidence was 77

    2026Diabetologia(2026)引用:67
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    3Kisspeptin-10 Regulates Glycosaminoglycan and Decorin Content in Human Cardiac Fibroblast Cultures
    Paulina Radwańska, Maciej Olkiewicz,Lucyna Piera,Jacek Drobnik

    Background Cardiac fibroblasts play a key role in extracellular matrix (ECM) remodelling through the synthesis of glycosaminoglycans and proteoglycans (PGs), such as decorin; however, the effects of kisspeptin-10 (KiSS-10) on these components in the heart remain unknown. The aim of this study was to determine the influence of KiSS-10 on glycosaminoglycan and decorin content in human cardiac fibroblast cultures and identify its mechanism. Methods The effects of KiSS-10 on glycosaminoglycans and decorin were assessed in human cardiac fibroblast cell line, with or without signalling inhibitor. Glycosaminoglycan levels were determined by the Farndale method, decorin secretion by enzyme-linked immunosorbent assay (ELISA), and decorin expression by quantitative polymerase chain reaction (qPCR). Results KiSS-10 treatment caused a dose-dependent increase in glycosaminoglycan content in both cells and medium. This stimulatory effect was abolished by blocking G-protein-coupled receptor 54 (GPR54) with peptide 234 or focal adhesion kinase (FAK) with FAK inhibitor 14 (FAKi). Combining KiSS-10 with phospholipase C inhibitor (D609) did not alter the glycosaminoglycan level compared to KiSS-10 alone. KiSS-10 increased decorin secretion but not expression. Combining peptide 234 with KiSS-10 did not alter media decorin level compared to KiSS-10 alone. Conclusions KiSS-10 significantly elevated glycosaminoglycan and decorin accumulation in human cardiac fibroblast cultures. This regulatory effect on glycosaminoglycan level appears to be dependent on GPR54 activation and FAK signalling, but not on phospholipase C function. Hence, KiSS-10 may be involved in ECM remodelling in the heart.

    2026Pharmacological Reports(2026)引用:49
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    4Preclinical Efficacy of Drug Delivery Systems in Colon Cancer Therapy: a Systematic Review and Meta-Analysis of in Vivo Animal Studies.
    Rozafa Koliqi, Arlinda Daka Grapci, Michael Y. Henein, Agata Bielecka-Dabrowa, Ibadete Bytyçi

    Abstract Background Drug delivery systems (DDS) offer a promising strategy to enhance the therapeutic index of chemotherapeutic agents in colon cancer by improving tumor targeting, circulation time, and controlled drug release. Despite extensive preclinical research, a quantitative synthesis evaluating the efficacy of DDS and the influence of design parameters remains lacking. Methods We conducted a systematic review and meta-analysis of preclinical in vivo studies assessing DDS-based chemotherapy in murine models of colon cancer. A comprehensive search of PubMed, EMBASE, Scopus, Google Scholar, Cochrane CENTRAL, and ClinicalTrials.gov was performed through October 15, 2025. Outcomes included tumor growth inhibition, with subgroup analyses examining the effects of DDS platform, chemotherapeutic agent, targeting strategy, ligand type, and route of administration. Results Twenty-three studies comprising 25 experiments and 539 animals were included. Overall, DDS-based therapies significantly reduced tumor growth compared with controls ((WMD: − 557.7; 95% CI: − 716.8 to − 398.5; I²=88%; p < 0.001) and free-drug administration ((WMD: − 276.3; 95% CI: − 367.6 to − 185.1; I²=78%; p < 0.001). Both targeted and non-targeted DDS significantly reduced tumor growth compared with free drug treatment, while targeted DDS showed significantly greater efficacy than non-targeted systems (WMD: − 240.3; 95% CI: − 399.4 to − 81.25; I²=59%; p = 0.003). Although no statistically significant differences were observed between DDS platforms or chemotherapeutic agent subgroups, micelle-based systems and DDS formulations incorporating SN-38 or doxorubicin tended to show greater tumor growth reduction. Intravenous administration demonstrated significantly greater efficacy than intraperitoneal delivery, while hyaluronic acid- and aptamer-based targeting strategies achieved the largest tumor growth inhibition. Risk-of-bias assessment indicated moderate methodological quality, with variability in reporting of randomization, blinding, and sample size calculations. Conclusions DDS-based chemotherapy consistently improves antitumor efficacy in preclinical colon cancer models, with targeting strategy, platform type, chemotherapeutic agent, and administration route influencing outcomes. These findings support the rational design of DDS platforms and underscore their translational potential. Rigorous preclinical study design and standardized reporting of efficacy and safety are essential to facilitate clinical translation.

    2026Journal of the Egyptian National Cancer Institute(2026)引用:40
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    5Selective Non-Operative Management of Post-Appendectomy Abscesses in Children: a Comprehensive Systematic Review and Pairwise Meta-Analysis
    Agata Grochowska, Kirti Kumar Hinduja, Alana Larissa Aparecida Marques, Laura Helena Fuenmayor Mena, Vyronas Argyris, Ana Emília Carvalho de Paula, Fernando Estima Seabra Neto, Alexia Rosas, Zarpana Akbari, Halima Sah, Miguel Eduardo Rodriguez, Camila Santos Loor,

    Post-appendectomy intra-abdominal abscess remains a common complication following pediatric appendicitis. Although drainage has traditionally been considered standard treatment, increasing evidence suggests selected patients may be successfully managed with antibiotics alone. A systematic review and meta-analysis were conducted in accordance with PRISMA guidelines and registered in PROSPERO (CRD420251075191). PubMed, Embase, and the Cochrane Central Register of Controlled Trials were searched through June 20, 2025. Eligible studies included pediatric patients (0–18 years) with post-appendectomy abscess managed with antibiotic vs. invasive drainage. The primary outcome was failure of first-line treatment requiring escalation. Secondary outcomes included recurrence and length of hospital stay. Ten observational studies involving 363 pediatric patients were included (152 drainage, 211 conservative). Treatment success was 80.9

    2026Pediatric Surgery International(2026)引用:16
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