Background: Esophageal perforation is a life-threatening condition of a complex etiology. No clear guidelines are available regarding the management of this condition. In this study, we review publications related to esophageal perforation, and analyze patients treated for this condition at our Department of Thoracic, General and Oncological Surgery. Objective: The objective of the study was to retrospectively assess and analyze management methods for esophageal perforations of different etiologies. All patients were treated in the Department of Thoracic, General and Oncological Surgery in years 2009-2015. Patients with perforations resulting from post-operational leaks within surgical anastomoses were excluded from the study. Material, methods, results: The analysis involved a total of 16 cases of esophageal ruptures. All cases were treated in years 2009-2015. Patients with perforations resulting from postoperative leaks within surgical anastomoses following elective surgeries for either oncological or non-oncological causes were excluded. The most common reason for esophageal rupture was iatrogenic injury (7 cases, 44%). Other causes included Boerhaave syndrome (5 cases, 31.2%), blunt trauma (2 cases, 12.5%), abscess perforation (1 case, 6.2%), and ulcer perforation (1 case, 6.2%). Ten patients underwent surgery, and the rest underwent esophageal prosthesis placement, of whom 2 cases required drainage of the mediastinum and pleural cavity. The mortality rate in the study group was 9/16 cases (56.2%). Conclusions: Esophageal perforation poses a significant interdisciplinary challenge regarding diagnostic workup, selection of treatment methods, and management of potential postoperative complications. This retrospective study was conducted in a single center. Although the analyzed period was long, we found only 16 cases. In spite of a variety of etiologies present, we found several statistically significant results of potential clinical value. 1. Most perforations that are not diagnosed within 48 hours affected the lower part of the esophagus and presented with unclear symptoms and imaging findings 2. Delaying diagnosis and treatment beyond 24 hours was associated with a higher mortality rate.

The present study examines the relationship between circular RNA (circRNA) derived from three genes of the family a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTSs): ADAMTS6, ADAMTS9 and ADAMTS12 and the host gene expression in non-small-cell lung cancer (NSCLC) with regard to various clinical factors. Notably, an association was identified between ADAMTS12 expression and specific circRNA molecules, as well as certain expression patterns of ADAMTS6 and its derived circRNA that were specific to histopathological subtypes. The survival analysis demonstrated that a lower ADAMTS6 expression in squamous cell carcinoma was associated with extended survival. Furthermore, the higher ADAMTS9 expression was linked to prolonged survival, while the overexpression of ADAMTS12 was correlated with a shorter survival. These findings suggest that circRNA molecules may serve as potential diagnostic or prognostic biomarkers for NSCLC, highlighting the importance of considering molecular patterns in distinct cancer subtypes.

In lung cancer patients, two complementary abnormalities were found that can cause disruption of the mitochondrial network: increased fusion and impaired fission, manifested by reduced levels of FIS1, a mitochondrial division regulator, and increased expression of MFN1, a mitochondrial fusion mediator. Immunoexpression studies of MFN1 and FIS1 proteins were performed in serum samples obtained from 47 patients with non-small cell lung cancer (NSCLC) and 21 controls. In the NSCLC patients, the immunoexpression of the MFN1 protein was significantly higher, and the FIS1 protein level was significantly lower than in the control group (p < 0.01; p < 0.001; UMW test). Patients with early, operable lung cancer had significantly lower levels of MFN1 immunoexpression compared to patients with advanced, metastatic lung cancer (p < 0.05; UMW test). This suggests that early stages of the disease are characterized by greater fragmentation of damaged mitochondria and apoptosis. In contrast, lower FIS1 protein levels were associated with a worse prognosis. Increased mitochondrial fusion in the blood of lung cancer patients may suggest an increase in protective and repair mechanisms. This opens up questions about why these mechanisms fail in the context of existing advanced cancer disease and is a starting point for further research into why protective mechanisms fail in lung cancer patients.

Background: Despite the decrease of morbidity rate of non-small cell lung cancer (NSCLC) in recent years, it is still a cancer with poor prognosis. Lung cancers (LCs) are usually diagnosed at a late stage of the disease due to non-specific clinical symptoms. Proper regulation of carnitine levels is important in the context of development and increased risk of cancer cells proliferation. The expression profiles and clinical value of SLC family members in LC remain largely unexplored. The aim of the study was the assessment of SLC22A16, SLC22A5 and SLC6A14 mRNA expression level among patients suffering from NSCLC. The obtained results were compared with the clinical and the pathological features of NSCLC patients. Methods: Through reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and bioinformatics studies, the evaluation of carnitine transporting genes (SLC22A16, SLC22A5 and SLC6A14) mRNA levels was performed in order to elucidate their connection to clinical features of patients and influence on overall survival (OS). Results: The analysis showed a significant difference for the SLC22A5 gene of NSCLC patients and for SLC6A14 and SLC22A5 genes in LUSC patients in terms of sex (P=0.002, P=0.02 and P=0.001, respectively) and in terms of tobacco smoking (P=0.04). Analysis also revealed a significant negative correlation for SLC22A5 and SLC22A16 genes expression level in the lung adenocarcinoma (LUAD) subtype with standardized uptake value (SUV) (r=−0.40, P=0.02 and r=−0.43, P=0.04). The significant downregulation of gene expression compared to normal adjacent tissue was observed for SLC22A5 in lung squamous cell carcinoma (LUSC) and for SLC6A14 in both LUAD and LUSC subtypes. The effect of the SLC22A5, SLC22A16 and SLC6A14 gene expression at the time of diagnosis on the OS time of LC patients revealed that lower expression correlated with a shorter 5 years OS (all P values <0.01). The effects were distinct after division for LUAD and LUSC subtypes. Conclusions: The expression levels of genes encoding carnitine transporters are diverse, hinting at a potentially altered carnitine metabolism in LC patients. Notably, this variance is not uniform and exhibits specificity across LC subtypes, with marked distinctions between LUAD and LUSC. The correlation between gene expression levels and OS of patients underlines the prognostic significance of SLC genes within these cancer subtypes.

Introduction : Oxidative stress appears to play an essential role as a secondary messenger in such physiological processes as apoptosis and survival as well as in proliferative signaling pathways. Oxidative damage is also considered to play a pivotal role in ageing, several degenerative...

TBC1D1 and TBC1D4 proteins play analogous, but not identical role in governing insulin-signalling pathway. Little is known about changes in expression levels of TBC1D1 and TBC1D4 genes in mammals, including humans. Number of factors were studied, but data remain controversial. The aim of this study was to evaluate the effect of selected cytokines, adipokines and myokines with known or putative insulin sensitivity regulation activity (adiponectin, irisin, omentin, interleukin 6, leptin, resistin, and tumour necrosis factor) on TBC1D1 and TBC1D4 expression levels in cultured differentiated human adipocytes. No significant differences were found between the adipocytes treated with different stimuli and this effect was determined not dose dependent. It is reasonable to conclude that relative shortage of data showing no change in TBC1D1 and TBC1D4 from literature results from publication bias; therefore, our finding provides additional insight into the role of both genes.