Introduction: Oral candidiasis is a common opportunistic fungal infection of the oral mucosa, most frequently caused by Candida albicans. Its development is influenced by local factors, such as denture use and oral hygiene, as well as systemic conditions including diabetes, nutritional deficiencies, and chronic inflammatory diseases. Accurate diagnosis requires both clinical evaluation and mycological testing. The aim of this retrospective study was to analyze demographic characteristics, predisposing factors, and the species distribution of Candida isolates in patients diagnosed with oral candidiasis. Materials and Methods: A retrospective review of medical documentation was conducted to evaluate patient demographics, risk factors, comorbidities, denture use, and results of mycological examinations confirming oral candidiasis. Results: A total of 71 patients (49 women and 22 men), aged 21-85 years (mean 59.6 ± 16 years), were included in the study. Fungal etiology was confirmed in all cases, with Candida albicans identified most frequently (81.69%). Among comorbidities, cardiovascular diseases were most common (30.99%), followed by diabetes (14.08%), and chronic periodontitis, respiratory, and gastrointestinal diseases (each 11.27%). Removable dentures were used by 18.30% of patients, and nicotine addiction was reported in 9.86%. All strains were susceptible to the tested antifungals, except for species with known intrinsic resistance. Conclusions: Oral candidiasis in this cohort predominantly affected women and older adults, with Candida albicans remaining the most common etiological agent. Denture use emerged as an important local predisposing factor and was associated with a higher proportion of infections caused by non-albicans species. These findings underscore the importance of comprehensive clinical evaluation and routine mycological testing to guide targeted antifungal therapy, especially in patients with risk factors such as denture use or systemic comorbidities.

Cytomegalovirus (CMV) seropositivity associates with cardiovascular disease in healthy adults, but associations are unclear in people living with HIV (PLWH) despite their high CMV burden. However, CMV antibody levels correlated with inflammatory biomarkers only in PLWH who subsequently developed coronary artery disease (CAD), so the effects of CMV in an individual may vary. Here we investigate the role of CMV-encoded interleukin-10 (cmvIL-10) in PLWH on anti-retroviral therapy. Plasma levels of cmvIL-10 and antibodies reactive with a cmvIL-10 peptide or a lysate of CMV-infected fibroblasts were assessed in PLWH with or without CAD. cmvIL-10 was assessed at diagnosis/selection (T0) and 12 months earlier (T-12), with anti-cmvIL-10 also assessed at -24 and -36 months (n = 36-58/group). Plasma cmvIL-10 was recorded as positive in 5-10 PLWH per group, irrespective of CAD status. Of 21 PLWH with detectable cmvIL-10, only six were positive at both timepoints. Anti-cmvIL-10 was measurable in all samples, at levels independent of cmvIL-10, CAD or time of sampling. Amongst PLWH without CAD, the detection of cmvIL-10 associated with higher levels of CXCL10 (T0 and T-12) and lower levels of the IL-1 receptor antagonist (IL-1Ra; T0 only). At T-12, anti-cmvIL-10 correlated with IL-1Ra in PLWH without CAD (p = 0.01), and sCD14 in PLWH with CAD (p = 0.01). Anti-cmvIL-10 correlated with VCAM-1 at several timepoints in both groups. Hence, cmvIL-10 may be produced episodically, inducing anti-cmvIL-10 peptide antibody, which may represent levels of the cytokine averaged over time. Plasma levels of cmvIL-10 and anti-cmvIL-10 antibody associated differently with inflammatory biomarkers in PLWH with and without CAD, suggesting mechanisms by which host responses to CMV may have different clinical consequences.

Borrelia burgdorferi sensu lato is a complex of spirochetes that includes the main pathogenic species B. burgdorferi sensu stricto, B. afzelii, and B. garinii, the causative agents of Lyme disease. Our aim was to determine the seroprevalence of anti-Borrelia IgG antibodies and assess associated risk factors among blood donors from Western Romania. We conducted a cross-sectional study of 1347 consecutive donors at the Regional Blood Transfusion Center in Timisoara, Western Romania, between November and December 2018. Participants completed an epidemiological questionnaire and serum samples were tested for IgG antibodies against B. burgdorferi sensu lato using the VIDAS^® Lyme IgG assay. The overall seroprevalence was 2.08% (28/1347). Individuals aged 46-55 years had the highest prevalence (3.79%) and a more than fivefold increased risk compared to those aged 18-25 years (aOR = 4.77; 95% CI: 1.24-18.27; p = 0.023). Soil exposure was also independently associated with higher seropositivity (aOR = 2.37; 95% CI: 1.10-5.09; p = 0.027). Other factors, including residence, gender, and pet ownership, showed no significant associations. Our findings provide new epidemiological data for Romania and emphasize the importance of environmental exposures in shaping Borrelia seroprevalence.

Cardiovascular diseases and metabolic dysfunction-associated steatotic liver disease (MASLD) are increasing sharply worldwide and share overlapping pathophysiological pathways, including oxidative stress, inflammation, hyperglycemia, obesity, dyslipidemia, and hypertension. Dark chocolate, rich in cocoa flavanols such as epicatechin and catechin, exhibits antioxidant and anti-inflammatory effects. Based on these properties, this narrative review uniquely integrates evidence on chocolate's effects on both cardiovascular and hepatic health, exploring shared mechanisms and clinical implications. Evidence from clinical studies suggests that chocolate modulates nitric oxide bioavailability and NADPH oxidase activity. Clinical findings demonstrate improvements in flow-mediated dilation, decreased NT-proBNP, reduced intestinal permeability and endotoxemia, improved lipid profile (increased HDL-c and reduced total cholesterol, LDL-c, and triglycerides), increased plasma polyphenols, improved platelet function, and attenuated hepatocyte apoptosis. These findings suggest a potential role for cocoa flavanol-rich dark chocolate in cardiometabolic health; however, the evidence remains preliminary and is limited by heterogeneous study designs, small sample sizes, and short intervention durations. Despite these limitations, current evidence supports the inclusion of moderate dark chocolate consumption as a possible adjunct strategy to mitigate cardiometabolic and hepatic metabolic risks. Further large-scale, long-term trials are needed to confirm these beneficial effects and to standardize the dosage and formulation of cocoa flavanols.

Therapeutic prone positioning is widely used to improve oxygenation in patients with acute respiratory distress syndrome but is associated with an increased risk of pressure injuries, particularly affecting facial and anterior body regions.

This systematic review was conducted according to PRISMA 2020 and Joanna Briggs Institute guidelines and was prospectively registered in PROSPERO (CRD42023442604). PubMed, CINAHL, Web of Science, Scopus, and the Cochrane Library were searched from inception to June 2025, including grey literature. Primary studies involving adult, mechanically ventilated patients undergoing therapeutic prone positioning and evaluating pressure injury prevention strategies were included. Methodological quality was assessed using JBI critical appraisal tools. Owing to clinical and methodological heterogeneity, findings were synthesized using a Synthesis Without Meta-analysis (SWiM) approach.

Eight studies with heterogeneous designs were included. Preventive interventions mainly comprised prophylactic dressings, repositioning and support devices, and comprehensive care bundles. Most strategies were associated with a reduction in pressure injury incidence, particularly in facial and anterior anatomical areas. Greater effectiveness was observed when interventions were implemented within structured protocols supported by staff training and multidisciplinary coordination.

Preventive strategies appear effective in reducing pressure injuries associated with prone positioning in critically ill patients. The implementation of standardized, bundled prevention protocols may improve patient safety in intensive care settings.

Antibiotic-induced dysbiosis has been increasingly implicated in a range of pediatric outcomes, yet the concept remains variably defined and often inconsistently applied. The purpose of this review is to provide an overview and critical evaluation of the available data regarding the effects of early-life exposure to β-lactam antibiotics on the developing microbiome. We conducted a narrative review of experimental and epidemiological studies examining β-lactam exposure during pregnancy, the perinatal period, and early childhood was conducted. β-lactams induce reproducible alterations in microbial composition, diversity, and metabolic function, including decreases in Bifidobacterium and Lactobacillus and a relative increase in Enterobacteriaceae and other facultative anaerobes, especially in early life. Reduced microbial diversity and changed short-chain fatty acid-producing taxa often accompany these compositional changes. However, associations with immune, metabolic, and neurodevelopmental outcomes are heterogeneous and frequently confounded by indication host-related factors. Evidence for causality in humans remains limited despite strong mechanistic support from animal models. Current data support cautious interpretation, even though β-lactam-associated microbiome perturbations may contribute to disease susceptibility during vulnerable developmental windows. While mechanistic and longitudinal evidence continues to develop, antibiotic stewardship focused on appropriate indication and duration is still crucial.

Background/Objectives: Cardiac resynchronization therapy (CRT) is a cornerstone treatment for heart failure with reduced ejection fraction (HFrEF), yet many patients remain symptomatic despite long-term electrical optimization. Although sacubitril/valsartan (ARNI) is central to guideline-directed medical therapy (GDMT), data on its late initiation in patients with chronic CRT are scarce. This study evaluated the impact of delayed ARNI initiation on clinical status, functional capacity, and cardiac remodelling in a real-world CRT population. Methods: We performed a single-centre, retrospective observational study including 76 HFrEF patients with chronic CRT who started ARNI between 2022 and late 2024. Patients underwent standardized assessment at baseline (T0) and after 12 ± 3 months (T1), including clinical evaluation, 12-item Kansas City Cardiomyopathy Questionnaire (KCCQ-12), symptom-limited bicycle exercise testing, and comprehensive echocardiography. The primary endpoint was change in quality of life (QoL). Secondary endpoints included exercise capacity, echocardiographic reverse remodelling, NYHA class, loop diuretic dose, and device-detected arrhythmias. Dose-response and multidimensional response patterns were explored. Results: KCCQ-12 increased from 52.96 ± 16.33 to 75.55 ± 18.12 (Δ +22.59 ± 13.22, p < 0.001), with 89.5% achieving a clinically meaningful improvement. Exercise duration and peak workload improved significantly. LVEF increased from 35.08 ± 6.96% to 43.18 ± 8.42% (Δ +8.11%, p < 0.001), with reductions in left ventricular and atrial volumes. Loop diuretic dose decreased (median -10 mg/day furosemide equivalent, p < 0.001), and 26.3% discontinued diuretics. A lower prevalence of device-detected arrhythmias was observed at follow-up, from 34.2% to 6.6% (p < 0.001). Higher ARNI doses were associated with greater likelihood of clinical, functional, and structural response. Longer CRT duration reduced the probability of structural remodelling but not symptomatic or functional benefit. Conclusions: In patients with long-standing CRT, delayed ARNI initiation was associated with improvements in QoL, exercise capacity, cardiac remodelling, congestion status, and electrical stability. These findings suggest that CRT is not a therapeutic ceiling and that late ARNI initiation remains a valuable component of comprehensive GDMT.

Pericardial cysts (PCs) are rare, benign congenital abnormalities that are encountered as mediastinal lesions. Despite their rarity, they remain clinically important due to their potential to mimic other mediastinal or cardiac pathologies and their capacity, in select cases, to cause significant complications. PCs are typically identified incidentally on imaging studies such as chest x-ray or transthoracic echocardiography, as most patients remain asymptomatic throughout their lives. When symptoms do occur, they are often nonspecific and related to compression of adjacent structures. Serious complications-including infection, rupture, and, rarely, cardiac tamponade-have been reported, underscoring the importance of accurate diagnosis and appropriate follow-up. Definitive characterization of PCs is best achieved using advanced imaging modalities such as cardiac computed tomography or cardiac magnetic resonance imaging, which help differentiate PCs from other mediastinal masses. While many PCs remain stable or even regress spontaneously, intervention may be warranted for symptomatic patients, enlarging cysts, or when the diagnosis remains uncertain. Therapeutic options include percutaneous aspiration, which carries a risk of recurrence, and surgical resection, which offers definitive treatment with excellent outcomes. This review provides a comprehensive overview of the etiology, clinical manifestations, diagnostic evaluation, differential diagnosis, complications, and management strategies for PCs.

Background: Aortic stiffness (AoS) is an established predictor of cardiovascular morbidity and mortality. Endovascular aneurysm repair (EVAR) introduces a rigid stent-graft into the aorta, potentially increasing AoS and impairing subendocardial perfusion. This prospective study aimed to evaluate changes in AoS and myocardial perfusion following EVAR, measured by carotid-to-femoral pulse wave velocity (cf-PWV) and the Subendocardial Viability Ratio (SEVR), and examined the influence of graft length on post-operative cf-PWV and SEVR. Methods: From October 2023 to April 2025, 38 patients undergoing elective EVAR were prospectively enrolled. Cf-PWV and the SEVR were measured <72 h preoperatively and 7 days postoperatively using the PulsePen^® device. Descriptive statistics were used to summarize baseline characteristics. Data were assessed for normality with the Shapiro-Wilk test; non-normally distributed variables were analysed using the Wilcoxon signed-rank test and presented as median [interquartile range, IQR], while normally distributed variables were analysed using paired t-tests and presented as mean ± standard deviation (SD). Linear regression was applied to evaluate associations between graft length and postoperative changes in cf-PWV and SEVR. Results: Cf-PWV increased significantly after EVAR, with a median within-patient change of 1.0 m/s [IQR 3.1] (p < 0.001), corresponding to a 10.6% increase. The SEVR decreased significantly by 15.1% (p = 0.006). Graft length correlated positively with cf-PWV change, with a 0.2% increase in cf-PWV per millimetre of graft length (r = 0.41; p = 0.029), but not with SEVR (r = 0.058, p = 0.763). Conclusions: EVAR was associated with increased AoS and reduced subendocardial perfusion, with greater stiffness changes observed in patients receiving longer grafts. These preliminary findings highlight important haemodynamic consequences of EVAR and may inform patient selection, postoperative management, and the development of future stent-graft designs to mitigate long-term cardiovascular risk.

Background: Lung cancer and chronic obstructive pulmonary disease (COPD) are morbid and mortal conditions arising from noxious endothelial stress. Soluble Major Histocompatibility Complex I Chain Related A (sMICA) is an activating ligand for the NKG2C receptor, and the soluble form indicates endothelial stress and is a mechanism for evading immune surveillance in lung cancer. We provide independent associations between sMICA*008 levels and the prevalence of lung cancer, lung cancer histologies, COPD, and risk factors for both diseases. Methods: We describe statistical associations between sMICA and demographic and clinical variables. Multivariate linear regression determined the independent associations between sMICA levels and lung cancer histology, between those with and without primary lung cancer, and prevalent COPD in participants without lung cancer. Point estimates and 95% confidence intervals are reported; p < 0.05 is considered statistically significant. Results: The cohort (n = 586 patients) included 24% female and 48% current or former smokers. Mean sMICA were 5.20 pg/mL ×10², and FEV1%-predicted of 62. sMICA levels were higher in those who smoked vs. those who did not. In Multivariate regression, non-small cell lung cancer (NSCLC) was associated with 14.2 pg/mL ×10² (95% CI 3.57 to 24.9 pg/mL ×10²) higher sMICA levels compared to those without cancer. No other histology was independently associated with higher sMICA. Primary lung cancer [12.5 pg/mL ×10² (2.85 to 22.2 pg/mL ×10²)] and COPD in those without cancer [4.38 pg/mL ×10² (0.38 to 8.39 pg/mL ×10²)] were associated with higher sMICA. Conclusions: sMICA*008 is independently associated with NSCLC, primary lung cancer, and COPD, respectively, in a cohort of current, former, and never smokers with and without lung cancer. sMICA levels were also higher in smokers. This study provides a foundation for future studies on sMICA activity in lung cancer and COPD, and assessment of sMICA as a biomarker for lung cancer cell type and risk of lung function loss in COPD.