Emerging evidence suggests a critical role of the gut microbiome in modulating systemic immune responses, with increasing relevance in dermatological diseases. Chronic spontaneous urticaria (CSU), traditionally viewed as an isolated cutaneous disorder, is now recognized as a systemic immune condition involving complex interactions between innate and adaptive immunity, mast cell dysregulation, and non-IgE-mediated pathways. This review explores the gut–skin axis as a unifying concept linking intestinal dysbiosis to inflammatory skin diseases, including atopic dermatitis, psoriasis, rosacea, and acne. Special emphasis is placed on CSU, where altered gut microbial composition, characterized by reduced diversity, depletion of short-chain fatty acid-producing bacteria, and expansion of Proteobacteria, may contribute to increased intestinal permeability, systemic immune activation via toll-like receptors, and heightened mast cell sensitivity. We discuss findings from animal models demonstrating that gut microbiota modulation can attenuate mast cell hyperreactivity and reduce urticarial symptoms. In parallel, we examine clinical evidence supporting the potential role of probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation as adjunctive strategies in CSU management. Despite promising findings, challenges remain in translating microbiome research into effective therapies due to interindividual variability, the complexity of host–microbiome interactions, and a lack of standardized protocols. Future research should focus on identifying predictive microbial patterns and developing personalized microbiome-targeted interventions. Understanding the bidirectional gut–skin relationship may open new therapeutic avenues beyond symptomatic treatment, positioning the microbiome as a novel target in CSU and related inflammatory dermatoses.

Background: Gynecological cancers, including ovarian, cervical, and endometrial cancers, significantly affect both survival and reproductive health in women. Cancer treatments such as chemotherapy and radiotherapy can impair ovarian function, reducing oocyte quality and fertility potential. Objective: This review aims to evaluate how vitamins and antioxidants can enhance fertility and fertility preservation outcomes for women diagnosed with gynecological cancers, particularly in the context of assisted reproductive technologies (ART). Standard treatments for these cancers, including hysterectomy, bilateral salpingo-oophorectomy, radiation, and chemotherapy, often compromise ovarian function and oocyte quality. This review focuses on the potential role of these interventions in improving oocyte quality, thereby supporting successful fertility preservation and ART outcomes. Methods: A comprehensive narrative review of the current literature was conducted, examining the effects of vitamins A, C, D3, E, and Coenzyme Q10 on oocyte quality, particularly in the context of oxidative stress and inflammation induced by cancer and its treatments. Results: The evidence suggests that certain vitamins and antioxidants may mitigate oxidative damage and enhance oocyte quality. Vitamin A supports cumulus–oocyte complex integrity, while vitamins C and E act as potent antioxidants, reducing oxidative stress in ovarian tissues. Vitamin D3 enhances ovarian reserve markers and modulates inflammatory cytokines. Coenzyme Q10 improves mitochondrial function and reduces DNA damage, increasing oocyte viability and fertilization potential. Conclusions: The incorporation of specific vitamins and antioxidants into fertility preservation strategies may enhance oocyte quality in women with gynecological cancers. Although the preliminary findings are promising, further research is needed to determine optimal dosages and establish standardized protocols for clinical use.

Background/Objectives: Predicting post-COVID-19 diabetes is crucial for enhancing patient care and public health. This study investigates the role of metabolic factors in predicting the glycemic outcomes in patients recovering from moderate to severe COVID-19. Methods: We conducted a retrospective analysis of 135 patients without pre-existing diabetes, selected from a cohort of 1980 individuals hospitalized between January 2020 and December 2022. Metabolic parameters, including blood glucose, Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), Triglyceride/Glucose (TyG) index, and high-sensitivity C-reactive protein (hs-CRP), were assessed at discharge and followed up after 4 months (T4) and 12 months (T12). Results: Statistical analysis revealed significant correlations of initial glycemia, HOMA-IR, and hs-CRP with the subsequent glycemic levels at T4 and T12. Multiple regression analysis confirmed that initial glycemia, HOMA-IR, and hs-CRP were strong predictors of elevated glycemia, while the TyG index did not show a significant predictive value. Conventional diabetes risk factors, including body mass index (BMI) and lipid profiles, showed low predictive power for post-COVID-19 glycemia. Conclusions: This research highlights the critical role of metabolic and inflammatory pathways in managing glycemic control in COVID-19 patients. Markers like blood glucose, HOMA-IR, and hs-CRP are significant predictors of blood glucose levels, while the TyG index appears less helpful in this context. Early, targeted interventions based on these markers can improve patient outcomes and reduce the risk of post-COVID-19 complications like diabetes.

Hematopoietic stem cells have a remarkable plastic capacity, which allows them to differentiate into various cells, such as immune cells, nervous cells, muscle cells, bone and cartilaginous cells. The aim of this study was to show the capacity of stem cells to differentiate into endothelial cells, in culture, after addition of endothelial cells growth suplement (ECGS). We also compared the behavior of these cells with that of endothelial cells obtained from human umbilical vein (HUVEC). CD34+ cells obtained by immunomagnetic separation from human umbilical cord and placental blood were used. After 12‐15 days of culture in a medium containing ECGS, the cells showed morphological changes characteristic to endothelial cells and immunocytochemical analysis revealed the presence of CD31 surface antigen and von Willebrand factor. The flow‐cytometric analysis of endothelial cells adhesion molecules (ECAM) showed that endothelial cells derived from CD34+ cells expressed CD54/ICAM‐1 9.65 ± 0.2% and CD106/VCAM 7.73±0.3%, values similar to those expressed by HUVECs. After TNF incubation, ECAM expression increased only in HUVECs. These data demonstrate that a fraction of circulating CD34+ cells may develop some endothelial cell characteristics when cultured with ECGS, but they are functionally different from HUVECs.

Background: A growing body of evidence links a high-fructose diet (HFrD) to metabolic disturbances, including inflammation, dyslipidemia, insulin resistance and also endothelial dysfunction, yet its role in allergic asthma remains underexplored. Considering that obesity and hypercholesterolemia exacerbate asthma by promoting systemic inflammation, investigating interventions with dual metabolic and anti-inflammatory effects is essential. This study aimed to evaluate the potential modulatory effects of rosuvastatin in ameliorating the effects of HFrD-induced metabolic and vascular dysfunction in the context of allergic asthma. Methods: Forty-eight Sprague-Dawley rats were assigned to eight groups, receiving either a standard or HFrD for 12 weeks. Allergic asthma was induced using an ovalbumin sensitization and challenge protocol, while controls were administered saline. Selected groups were treated with rosuvastatin throughout the entire duration of the experiment. Body weight, abdominal circumference and serum biomarkers were assessed at baseline, 6 and 12 weeks. Endothelial function was assessed by evaluating vascular reactivity in an isolated organ bath. Additionally, histopathological analyses of aortic and pulmonary tissues were conducted to investigate inflammatory responses and morphological changes. Results: Rats on HFrDs exhibited significant increases in body weight, abdominal circumference, lipid profiles and blood glucose, which were further aggravated by allergic asthma. Rosuvastatin treatment notably reduced lipid levels, C-reactive protein and immunoglobulin E, while also enhancing vascular reactivity and attenuating aortic and bronchial wall thickening. Conclusions: Our findings suggest that rosuvastatin may serve as an effective therapeutic agent for addressing vascular and inflammatory complications associated with a high fructose intake and allergic asthma.

Progressive multiple sclerosis (PMS) represents a distinct clinical and biological entity characterized by compartmentalized neuroinflammation, chronic glial activation, and resistance to conventional immunotherapies. Unlike relapsing MS, PMS is sustained by resident CNS immune networks, where activated microglia and astrocytes orchestrate persistent cytokine signaling—particularly involving TNF-α, IL-1β, and IL-6—through self-amplifying feedback loops. In this narrative review, we explore how these cytokines interact with oxidative stress, iron accumulation, mitochondrial dysfunction, and impaired autophagy to drive neurodegeneration. Human-based evidence is integrated with insights from experimental models to clarify translational mechanisms. We also highlight fluid biomarkers (e.g., GFAP, NfL) and imaging modalities (e.g., TSPO-PET, QSM) that reflect glial activity and disease progression in vivo. Age, sex hormones, and immunosenescence are discussed as modulators of cytokine expression. Finally, we review emerging therapeutic strategies that target glial metabolism and cytokine networks rather than peripheral immune cells, offering a systems-based framework for future PMS interventions and personalized disease monitoring.