Abnormal glycosylation of cancer cells is considered a key factor of carcinogenesis related to growth, proliferation, migration and invasion of tumor cells. Many plant-based polyphenolic compounds reveal potential anti-cancer properties effecting cellular signaling systems. Herein, we assessed the effects of phenolic acid, p-coumaric acid and flavonoids such as kaempferol, astragalin or tiliroside on expression of selected cancer-related glycoforms and enzymes involved in their formation in AGS gastric cancer cells. The cells were treated with 80 and 160 µM of the compounds. RT-PCR, Western blotting and ELISA tests were performed to determine the influence of polyphenolics on analyzed factors. All the examined compounds inhibited the expression of MUC1, ST6GalNAcT2 and FUT4 mRNAs. C1GalT1, St3Gal-IV and FUT4 proteins as well as MUC1 domain, Tn and sialyl T antigen detected in cell lysates were also lowered. Both concentrations of kaempferol, astragalin and tiliroside also suppressed ppGalNAcT2 and C1GalT1 mRNAs. MUC1 cytoplasmic domain, sialyl Tn, T antigens in cell lysates and sialyl T in culture medium were inhibited only by kaempferol and tiliroside. Nuclear factor NF-κB mRNA expression decreased after treatment with both concentrations of kaempferol, astragalin and tiliroside. NF-κB protein expression was inhibited by kaempferol and tiliroside. The results indicate the rationality of application of examined polyphenolics as potential preventive agents against gastric cancer development.

Background: Rehabilitation is an effective method for improving the overall health of patients who have experienced the long-term effects of COVID-19. Methods: The double-blind, randomized prospective study assessed the effectiveness of a 6-week rehabilitation program among post-COVID-19 patients. A total of 59 patients under treatment following COVID-19 were randomly divided into two groups. Both groups completed the same six-week comprehensive exercise training program supported by a respiratory muscle trainer (Threshold IMT) during out-patient sessions. The control group performed placebo IMT. Respiratory muscle strength, chest wall expansion, spirometry, and diaphragm ultrasonography measurements were taken before and after the six weeks. Results: The applied rehabilitation program improved respiratory muscle strength in both the study and control groups (p < 0.001). There was a significant chest circumference increase in the study group (p < 0.001). Spirometric parameters improved in both groups, with the study group showing a greater improvement: 8.02% in FEV1 (p < 0.001), 13.24% in FVC EX (p < 0.001) and 9.67% in PEF (p < 0.001). Rehabilitation also increased diaphragm thickness during maximum inhalation in both groups. Conclusions: Based on the study findings, the specialized outpatient rehabilitation program developed for post-COVID-19 patients has proven to be effective and safe.

Pancreatic ductal adenocarcinoma (PDAC) is one of humans’ most common and fatal neoplasms. Nowadays, a number of PDAC studies are being conducted in two different fields: non-coding RNA (especially microRNA and long non-coding RNA) and microbiota. It has been recently discovered that not only does miRNA affect particular bacteria in the gut microbiome that can promote carcinogenesis in the pancreas, but the microbiome also has a visible impact on the miRNA. This suggests that it is possible to use the combined impact of the microbiome and noncoding RNA to suppress the development of PDAC. Nevertheless, insufficient research has focused on bounding both approaches to the diagnosis, treatment, and prevention of pancreatic ductal adenocarcinoma. In this article, we summarize the recent literature on the molecular basis of carcinogenesis in the pancreas, the two-sided impact of particular types of non-coding RNA and the pancreatic cancer microbiome, and possible medical implications of the discovered phenomenon.

Venous thromboembolism (VTE) is a prevalent and potentially fatal condition, typically initiating deep vein thrombosis (DVT). Subsequent embolization can lead to pulmonary embolism (PE), a significant threat to cardiovascular function. Approximately 5% of PE cases result in sudden cardiac arrest due to acute right ventricular failure, arrhythmias, and circulatory shock. Given the considerable influence of PE on right ventricular function, this study aimed to investigate alterations in gene expression within the right ventricle associated with PE in a porcine model. The study was performed on 12 male pigs, divided into two groups of six animals each. In the experimental group, a thrombus was induced in the right femoral vein of each animal and subsequently released to induce pulmonary embolism. The remaining six animals served as a control group. Right ventricular myocardial samples were collected for subsequent transcriptomic and immunohistochemical analyses. In the experimental group, tissue samples were taken 24 h post-thrombus release to characterize changes typical of acute PE. Multistep bioinformatics identified 1992 significantly differentiating molecules: 1436 differentially expressed genes (DEGs), 308 differentially expressed lncRNAs (DELs), and 248 other RNA species. Among these, 417 DEGs, 101 DELs, and 58 other RNAs were downregulated, while 1019 DEGs, 207 DELs, and 190 other RNAs were upregulated. Gene Ontology (GO) analysis assigned molecules to 259 processes (184 biological, 37 cellular, 33 molecular), indicating active inflammatory and immune signaling in cardiac tissue, suggesting roles in ventricular remodeling and stress response. KEGG pathway analysis highlighted altered Oxytocin signaling and Complement and coagulation cascades in PE hearts. Splicing analysis revealed 55,950 alternative splicing events in Sus scrofa right ventricles (PE vs. CTR). Additionally, 3142 single nucleotide variants (SNVs) were identified. This study presents the first comprehensive analysis of right ventricular gene expression profiles in response to PE. The findings indicate that alterations in the oxytocin signaling pathway, the complement and coagulation cascades, and disturbed inflammatory and immune signaling are critically involved in the pathogenesis of right ventricular dysfunction during PE.