Cardiac macrophages are known from various activities, therefore we presume that microRNAs (miRNAs) produced or released by macrophages in cardiac tissue have impact on myocardial remodeling in individuals with metabolic syndrome (MetS). We aim to assess the cardiac macrophage miRNA profile by selecting those miRNA molecules that potentially exhibit regulatory functions in MetS-related cardiac remodeling. Cardiac tissue macrophages from control and db/db mice (an animal model of MetS) were counted and sorted with flow cytometry, which yielded two populations: CD45⁺CD11b⁺CD64⁺Ly6C^hi and CD45⁺CD11b⁺CD64⁺Ly6C^low. Total RNA was then isolated, and miRNA expression profiles were evaluated with Next Generation Sequencing. We successfully sequenced 1400 miRNAs in both macrophage populations: CD45⁺CD11b⁺CD64⁺Ly6C^hi and CD45⁺CD11b⁺CD64⁺Ly6C^low. Among the 1400 miRNAs, about 150 showed different expression levels in control and db/db mice and between these two subpopulations. At least 15 miRNAs are possibly associated with MetS pathology in cardiac tissue due to direct or indirect regulation of the expression of miRNAs for proteins involved in angiogenesis, fibrosis, or inflammation. In this paper, for the first time we describe the miRNA transcription profile in two distinct macrophage populations in MetS-affected cardiac tissue. Although the results are preliminary, the presented data provide a foundation for further studies on intercellular cross-talk/molecular mechanism(s) involved in the regulation of MetS-related cardiac remodeling.

Background: The need for safe and efficient dissemination of minimally invasive approach in liver surgery is among the current challenges for hepatobiliary surgeons. After the stage of innovators and pioneers, the following countries should adopt a laparoscopic approach. The aim of this study was to assess the national experience and trend in implementing laparoscopic liver resection (LLR) in Poland. Materials and methods: A national registry of LLR performed in Poland was established in June 2020. All LLR cases performed before were included retrospectively, followed by prospectively collected new cases. Baseline characteristics, preoperative and intraoperative data, short-term results and long-term follow-up were recorded. Results: Since 2010 up to the end of 2022 there were 718 LLRs performed in Poland. The national rate of laparoscopic approach has gradually increased since 2017 (P<0.001), reaching the rate of 11.7% in 2022. There were 443 (61.7%), 107 (14.9%), and 168 (23.4%) LLRs performed in accordance to increasing grades of difficulty. The move towards more demanding cases had an increasing trend over the years (P<0.001). Total intraoperative adverse event and postoperative severe complications rates were estimated for 13.5% (n=97) and 6.7% (n=48), respectively. 30-day reoperation, readmission and postoperative mortality rates were 3.6% (n=26), 2.8% (n=20), and 0.8% (n=6), respectively. While the R0 resection margin was assessed in 643 (89.6%) cases, the total textbook outcomes (TO) were achieved in 525 (74.5%) cases. Overcoming the learning curve of 60 LLRs, resulted in an increasing TO rate from 72.3 to 80.6% (P=0.024). Conclusions: It is the first national analysis of a laparoscopic approach in liver surgery in Poland. An increasing trend of minimizing invasiveness in liver resection has been observed. Responsible selection of cases in accordance with difficulty may provide results within global benchmark values and textbook outcomes already during the learning curve.

Metabolic syndrome (MetS) is a condition that includes symptoms, such as obesity, hyperglycemia, and hypertension, which elevate cardiovascular risk. An impaired angiogenic response of endothelial cells (ECs) in heart and peripheral organs has been proposed in MetS, but the mechanisms of this phenomenon have not been thoroughly explored. Results obtained from evaluating the whole myocardium are inconsistent, since different types of cells react differently to MetS environment and a variety of molecular pathways are involved in the angiogenic response. Therefore, the aim of this paper was to study one selected pathway—the VEGF/VEGFR pathway, which regulates the angiogenic response and microvascular permeability in ECs isolated from db/db mouse hearts. The expression of mRNAs for VEGF/VEGFR axis proteins was assessed with RT-PCR in ECs isolated from control and db/db mouse myocardium. The density of CD31-, VEGFR2-, and VE-cadherin-positive cells was examined with confocal microscopy, and the ultrastructure of ECs was analyzed with transmission electron microscopy. The aortic ring assay was used to assess the capacity of ECs to respond to angiogenic stimuli. Our results showed a decreased number of microvessels, diminished expression of VE-cadherin and VEGFR2 and widened gaps between the ECs of microcapillaries. The aortic ring assay showed a diminished number of sprouts in db/db mice. These results may indicate that ECs in MetS enhance the production of mRNA for VEGF/VRGFR axis proteins, yet sprout formation and vascular barrier maintenance are limited. These novel data may provide a foundation for further studies on ECs dysfunction in MetS.

Cardiac lymphatic vessels (LyVs) are suggested to be important players in cardiovascular disease-associated myocardial remodeling. However, there is a gap in the knowledge of whether LyV remodeling is an integral component of cardiac remodeling, especially in obesity associated with other comorbidities, including increased levels of circulating angiotensin II (Ang II). We studied the structural alterations in the myocardium and LyVs in Ang II-treated db/db mice compared with db/db mice and Ang II-treated wild-type mice with histopathological imaging methods, confocal microscopy, ultrastructural morphology, and morphometric analysis. We demonstrated that Ang II-treated db/db mice exhibited significantly increased fibrosis, cardiomyocyte hypertrophy, and local edema compared with untreated db/db mice; however, the cardiomyocyte hypertrophy was similar to that in Ang II-treated control mice. The decreased density of the LyVs and their wall shape alterations, with disorganized anchoring filaments, widened junctional gaps, decreased numbers of cytoplasmic vesicles indicative of a leaky phenotype, and increased basement membrane (BM) thickness, were observed in Ang II-treated db/db mice compared with Ang II-treated controls. Our findings revealed a structural basis for intensive LyV remodeling in association with cardiac remodeling in obesity.

Background/Objectives: The shortage of liver grafts remains a major challenge in transplantation. Full-left-full-right (FLFR) split liver transplantation (SLT) expands the donor pool by providing two grafts for small adult recipients. However, prolonged cold ischemia time (CIT) and ischemia-reperfusion injury (IRI) limit its success. Methods: We report a case of FLFR SLT utilizing ex situ dual hypothermic oxygenated machine perfusion (DHOPE) to mitigate IRI and enhance graft viability. A brain-dead donor’s liver was split under continuous DHOPE, followed by simultaneous transplantation into two adult recipients. Results: Both recipients exhibited stable graft function at one-year follow-up. DHOPE effectively reduced CIT and optimized postoperative recovery, with no major complications beyond Clavien–Dindo Grade IIIb. Conclusions: This is the first reported FLFR SLT using ex situ DHOPE for two adult recipients, demonstrating its feasibility in reducing CIT and improving outcomes. Machine perfusion may become a standard in FLFR SLT.

Background/Objectives: Metabolic syndrome (MetS) conditions lead to structural and functional alterations in cardiomyocytes, microvasculature, and extracellular matrix (ECM), leading to myocardial fibrosis and impaired diastolic function. Cardiac lymphatic vessels (LVs) are increasingly recognized as key regulators of myocardial homeostasis, yet their response to MetS remains poorly understood. Therefore, we aimed to investigate transcriptional changes in cardiac lymphatic endothelial cells (LECs) in db/db mice, a well-established model of MetS. Methods: Using flow cytometry-sorted LECs and RT-PCR, we analyzed mRNA expression of genes involved in lymphangiogenesis, metabolism, mechanotransduction, immune cell trafficking, and ECM interactions. Results: Our findings show the transcriptional plasticity of cardiac LECs in response to MetS. Conclusions: Although our study is limited by the lack of protein-level validation and functional assays, our approach provides a broader interpretative framework and identifies potential directions for future research, including functional studies and pathway-specific investigations of the identified genes to assess their impact on lymphatic flow and cardiac function. Understanding LEC responses to metabolic stress may uncover novel therapeutic targets for heart failure associated with MetS.