Obesity is a pandemic of the 21st century, and the prevalence of this metabolic condition has enormously increased over the past few decades. Obesity is associated with a number of comorbidities and complications, such as diabetes and cardiovascular disorders, which can be associated with severe and fatal outcomes. Adipose tissue is an endocrine organ that secretes numerous molecules and proteins that are capable of modifying immune responses. The progression of obesity is associated with adipose tissue dysfunction, which is characterised by enhanced inflammation and apoptosis. Increased fat-tissue mass is associated with the dysregulated secretion of substances by adipocytes, which leads to metabolic alterations. Importantly, the adipose tissue contains immune cells, the profile of which changes with the progression of obesity. For instance, increasing fat mass enhances the presence of the pro-inflammatory variants of macrophages, major sources of tumour necrosis factor α and other inflammatory mediators that promote insulin resistance. The pathogenesis of obesity is complex, and understanding the pathophysiological mechanisms that are involved may provide novel treatment methods that could prevent the development of serious complications. The aim of this review is to discuss current evidence describing the involvement of various inflammatory mediators in the pathogenesis of obesity.

Psoriasis is a chronic inflammatory skin disease, the prevalence of which is increasing. Genetic, genomic, and epigenetic changes play a significant role in the pathogenesis of psoriasis. This review summarizes the impact of epigenetics on the development of psoriasis and highlights challenges for the future. The development of epigenetics provides a basis for the search for genetic markers associated with the major histocompatibility complex. Genome-wide association studies have made it possible to link psoriasis to genes and therefore to epigenetics. The acquired knowledge may in the future serve as a solid foundation for developing newer, increasingly effective methods of treating psoriasis. In this narrative review, we discuss the role of epigenetic factors in the pathogenesis of psoriasis.

Cardiovascular diseases (CVDs) are the leading cause of death and include several vascular and cardiac disorders, such as atherosclerosis, coronary artery disease, cardiomyopathies, and heart failure. Multiple treatment strategies exist for CVDs, but there is a need for regenerative treatment of damaged heart. Stem cells are a broad variety of cells with a great differentiation potential that have regenerative and immunomodulatory properties. Multiple studies have evaluated the efficacy of stem cells in CVDs, such as mesenchymal stem cells and induced pluripotent stem cell-derived cardiomyocytes. These studies have demonstrated that stem cells can improve the left ventricle ejection fraction, reduce fibrosis, and decrease infarct size. Other studies have investigated potential methods to improve the survival, engraftment, and functionality of stem cells in the treatment of CVDs. The aim of the present review is to summarize the current evidence on the role of stem cells in the treatment of CVDs, and how to improve their efficacy.

Rheumatoid arthritis (RA) is a chronic and progressive autoimmune disease. The pathogenesis of RA is complex and involves interactions between articular cells, such as fibroblast-like synoviocytes, and immune cells. These cells secrete pro-inflammatory cytokines, chemokines, metalloproteinases and other molecules that together participate in joint degradation. The current evidence suggests the important immunoregulatory role of the gut microbiome, which can affect susceptibility to diseases and infections. An altered microbiome, a phenomenon known as gut dysbiosis, is associated with the development of inflammatory diseases. Importantly, the profile of the gut microbiome depends on dietary habits. Therefore, dietary elements and interventions can indirectly impact the progression of diseases. This review summarises the evidence on the involvement of gut dysbiosis and diet in the pathogenesis of RA.

Background: Herlyn-Werner-Wunderlich Syndrome is a rare malformation syndrome characterized by uterus didelphys with obstructed hemivagina and ipsilateral renal agenesis. Symptoms appear most often after menarche and are secondary to hematocolpos. We compare clinical symptoms, diagnosis and treatment of two patients, a 13-year-old and a 17-year-old. Case report: Despite the non-uniform clinical symptoms, it should be noted that in both patients, the 13-year-old and the 17-year-old, hematocolpos, which was probably the cause of lower abdominal pain, was diagnosed with ultrasound. The diagnosis was complemented by laparoscopy, which determined the diagnosis of malformation of uterus didelphys with obstructed hemivagina. The patients had a history of kidney agenesis, which, after gynecological diagnosis, turned out to be ipsilateral. In the 13-year-old, agenesis was diagnosed by uroscintigraphy, while in the 17-year-old it was diagnosed by urography. Incision and drainage of the residual vagina was performed in the course of therapeutic management. In both cases, the clinical situation required a repeated widening of the orifice. Conclusions: Lower abdominal pain accompanying hematocolpos suggested Herlyn-Werner-Wunderlich Syndrome (HWWS) as the cause of symptoms. 3D transvaginal ultrasound enabled the determination of a congenital uterine defect with high probability, although inconclusive cases required confirmation by laparoscopy. Incision of the blocked vagina and drainage of hematocolpos were the key components of treatment. The treatment of HWWS is a multi-step process.