Childhood obesity represents a worldwide concern as many countries have reported an increase in its incidence, with possible cardiovascular long-term implications. The mechanism that links cardiovascular disease to obesity is related to low-grade inflammation. We designed this study to investigate the diagnostic utility of inflammatory indices (NLR, neutrophil-to-lymphocyte ratio; PLR, platelet-to-lymphocyte ratio; SII, systemic immune-inflammation index; SIRI, systemic inflammation response index) in obese children with metabolic syndrome (MetS) and their relationship with cardiometabolic risk biomarkers, such as the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), triglyceride-to-high-density lipoprotein cholesterol (TG:HDL-C), and non-high-density lipoprotein cholesterol (non-HDL-C). A total of 191 obese children from one large Romanian reference center was included in the study. Patients were classified in two groups according to the presence (MetS group) or absence (non-MetS group) of metabolic syndrome. According to our results, the SII index proved to have diagnostic value in distinguishing MetS patients among children with obesity (AUC = 0.843, a sensitivity of 0.83, and a specificity of 0.63). Furthermore, the SII was positively associated with cardiometabolic risk biomarkers (HOMA-IR, p < 0.001; TG:HDL-C, p = 0.002; non-HDL-C, p = 0.021), highlighting its possible role as an additional measure of cardiometabolic instability in obese children.
Pelvic organ prolapse is a frequent health problem in women, encountered worldwide, its physiopathology being still incompletely understood. The integrity of the pelvic-supportive structures is a key element that prevents the prolapse of the pelvic organs. Numerous researchers have underlined the role of connective tissue molecular changes in the pathogenesis of pelvic organ prolapse and have raised the attention upon oxidative stress as an important element involved in its appearance. The advancements made over the years in terms of molecular biology have allowed researchers to investigate how the constituent elements of the pelvic-supportive structures react in conditions of oxidative stress. The purpose of this paper is to underline the importance of oxidative stress in the pathogenesis of pelvic organ prolapse, as well as to highlight the main oxidative stress molecular changes that appear at the level of the pelvic-supportive structures. Sustained mechanical stress is proven to be a key factor in the appearance of pelvic organ prolapse, correlating with increased levels of free radicals production and mitochondrial-induced fibroblasts apoptosis, the rate of cellular apoptosis depending on the intensity of the mechanical stress, and the period of time the mechanical stress is applied. Oxidative stress hinders normal cellular signaling pathways, as well as different important cellular components like proteins, lipids, and cellular DNA, therefore significantly interfering with the process of collagen and elastin synthesis.
Psoriasis is a T cell mediated, chronic inflammatory autoimmune skin disease that affects up to 2–3% of the global population and leads to a decrease in quality of life. Experimental data accumulated in recent years highlighted the important role played by the immune system in the pathogenesis of this disease. Non-human psoriasis models are an important research tool that attempts to reproduce the clinical features of the disease in order to explain the pathogenesis of psoriasis and to identify possible therapeutic targets. Imiquimod-based murine model of psoriatic dermatitis is an alternative to traditional models of experimental psoriasis in mice and the induced dermatitis closely mimics the pathologic changes in human psoriasis. In order to emphasize changes in immune cell populations involved in lesion pathogenesis, we performed a murine model of psoriasiform dermatitis model by topical IMQ application. The progress and the severity of IMQ-induced skin inflammation were clinically (PASI score) and histopathologically evaluated. The immunological changes induced by IMQ treatment in lymphocyte populations from peripheral blood and spleen were evaluated by flow cytometry. The main changes observed in peripheral blood were the significantly increased T-CD8a+ lymphocyte and NK1.1+ cell percentages and the decreased T-CD4+ and B lymphocyte percentages in IMQ-treated mice. In spleen samples, lymphocytes showed the same tendency of variation as in peripheral blood, but without statistical significance. A significant decrease of B cells percentages was observed in spleen suspensions. Data obtained in skin samples may suggest the involvement of CD3ε+, CD4+ and CD8a+ cells in the lesional process. This murine model was analyzed by performing a basic cellular profile at three levels: peripheral blood, spleen and skin. The evaluation aimed to establish the immune framework of this experimental model that could further be used for etipathogenic mechanism identification and/or for studies regarding targeted therapies.
Benign prostatic hyperplasia (BPH) is induced by a persistent local inflammatory process that leads to cell proliferation. Viral infections associated with immune deficiencies can trigger the chronic inflammation of the prostate. Therefore, we have investigated several viral expressions in BPH patients and tried to establish a link with the diagnosed hyperplasia. 50 patients with BPH without urinary tract infection were tested for the presence of the following viruses: human papilloma virus (HPV), cytomegalovirus (CMV) and Epstein-Barr virus (EBV). These viruses are the most common cause of asymptomatic viral infections. HPV-specific DNA detection by polymerase chain reaction (PCR) was used for freshly surgical removed tissue sample. Both anti-CMV (IgG, IgM) and anti-EBV (IgG, IgM) antibodies were detected in the patients� serum with standard enzyme-Linked Immunosorbent Assay technique (ELISA). Specific HPV-DNA in prostate tissue was found only in 4% of patients, while 98% and 100% patients were positive for serum anti-CMV IgG or anti-EBV, proving intense earlier contact with the virus. IgM anti-CMV evaluation was found in around 10% of the cases which were also negative for EBV, sustaining that this was a non-acute infection. The findings showed that BPH may be associated with a chronic inflammation due to the post-viral infection with CMV or EBV, or secondary to the presence of these viruses in the prostate, while the involvement of HPV infection in BPH development is comparably lower. Our data suggests that viral investigation in BPH should be considered in the screening protocol of BPH as an indicator of possible inflammatory-mediated tumorigenesis of urinary tract.
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