Background/Objectives : Recurrent incisional hernia remains a major challenge in abdominal wall surgery and is frequently associated with increased surgical complexity and adverse outcomes. However, its role as a distinct surgical entity and its cumulative operative impact remain insufficiently characterized. Methods: We conducted a retrospective cohort study including 1262 patients undergoing incisional hernia repair using the Rives–Stoppa technique between 2013 and 2022. Patients were stratified into primary and recurrent hernia groups. Operative burden was assessed using operative time and length of hospital stay. Results: Recurrent hernia was associated with a more adverse clinical profile, increased structural complexity, longer operative time, prolonged hospitalization, and higher postoperative complication rates. It remained independently associated with postoperative complications after adjustment for the principal measured confounders. Conclusions: Recurrent incisional hernia was associated with increased structural complexity, longer operative time, prolonged hospitalization, and worse postoperative outcomes compared with primary incisional hernia in patients undergoing elective retromuscular repair. Moreover, recurrent hernia remained independently associated with postoperative complications after adjustment for the principal measured confounders. These findings should be interpreted within the context of elective Rives–Stoppa repair and require external validation before broader clinical application.

Background: Mycosis fungoides (MF), the most prevalent cutaneous T cell lymphoma, features clonal CD4⁺ T cell proliferation within a Th2-dominant microenvironment. Interleukin-4 (IL-4) promotes disease progression while Brentuximab Vedotin (BV), an anti-CD30 antibody–drug conjugate, shows efficacy but faces resistance challenges. Methods: We conducted a narrative literature review (2010–2024) synthesizing evidence on IL-4 signaling and BV’s efficacy in MF to develop a theoretical framework for combination therapy. Results: IL-4 may modulate CD30 expression and compromise BV’s effectiveness through immunosuppressive microenvironment remodeling. Theoretical mechanisms suggest that IL-4 pathway inhibition could reprogram the microenvironment toward Th1 dominance and restore BV sensitivity. However, no direct experimental evidence validates this combination, and safety concerns including potential disease acceleration require careful evaluation. Conclusions: The proposed IL-4/BV combination represents a biologically compelling but unproven hypothesis requiring systematic preclinical validation and biomarker-driven clinical trials. This framework could guide future research toward transforming treatment approaches for CD30-positive MF by targeting both malignant cells and their immunologically permissive microenvironment.

Background/Objectives: Occupational burnout is a major challenge among healthcare workers. Night-shift work, insufficient sleep, and lifestyle factors may contribute to higher burnout levels. This study examined associations of night-shift work, sleep duration, and physical activity with burnout using the Burnout Assessment Tool (BAT). Methods: This cross-sectional study included 213 healthcare workers undergoing routine occupational health assessments in Bucharest, Romania, between January and April 2026. Burnout was assessed using the BAT-23 core questionnaire and BAT Secondary Symptoms module. Data on night-shift work, sleep duration, physical activity, age, sex, and professional experience were analyzed using group comparisons, correlations, and multivariable linear regression. Results: Night-shift workers had higher burnout scores than non-night-shift workers (3.36 ± 0.43 vs. 2.44 ± 0.41, p < 0.001), while physically active participants had lower scores than sedentary workers (2.46 ± 0.44 vs. 3.23 ± 0.52, p < 0.001). Burnout correlated negatively with sleep duration (r = −0.336, p < 0.001) and physical activity (r = −0.655, p < 0.001), and positively with night-shift work (r = 0.798, p < 0.001). In adjusted analysis, night-shift work (B = 0.831, 95% CI 0.637–1.024, p < 0.001), shorter sleep duration (B = −0.079, 95% CI −0.127 to −0.031, p = 0.001), and female sex (B = 0.162, 95% CI 0.029–0.295, p = 0.017; male = 0, female = 1) were associated with higher burnout; the model explained 58.6% of the variance. Conclusions: Night-shift work and shorter self-reported sleep duration were independently associated with higher burnout. Physical activity was associated with lower burnout only in unadjusted analyses. Owing to the cross-sectional design and self-reported exposures, findings should be interpreted as associations and confirmed longitudinally.

Background and Objectives: Rosacea is a chronic inflammatory dermatosis with a complex pathophysiology that continues to challenge effective long-term disease management. Rosacea is characterized by immune dysregulation, oxidative stress, neurovascular dysfunction, and impaired epidermal barrier integrity, while current therapeutic options remain limited. Hippophae rhamnoides (sea buckthorn) is a phytochemically rich medicinal plant with reported anti-inflammatory and dermo-reparative properties. Materials and Methods: A systematic literature review was conducted following PRISMA guidelines using the PubMed database. Studies published from 2020 onward evaluating sea buckthorn extracts, oils, or isolate bioactive compounds in the in vitro, in vivo, and limited clinical contexts were included, with emphasis on rosacea relevant mechanisms. Results: Twenty-six studies show that sea buckthorn compounds modulate inflammation, oxidative stress, vascular and immune responses, and barrier function in preclinical models. They consistently reduce pro-inflammatory mediators, improve barrier integrity, and attenuate immune or vascular activation, suggesting potential benefits for inflammatory skin disorders such as rosacea. Conclusions: Hippophae rhamnoides shows promising anti-inflammatory and skin-repairing effects that may benefit patients with rosacea. However, most evidence comes from preclinical studies, and clinical data specifically for rosacea are limited. Well-designed clinical trials are needed to confirm its effectiveness in treating this condition.

Bruton’s tyrosine kinase (BTK) inhibitors have revolutionized B-cell malignancy treatment but paradoxically increase infection susceptibility. Covalent BTK inhibitors (Ibrutinib, Acalabrutinib, Zanubrutinib) induce sustained BTK blockade but disrupt immune homeostasis through off-target effects on T-cell and myeloid signaling, contributing to hypogammaglobulinemia and increased risk of bacterial, viral, and opportunistic fungal infections. Non-covalent inhibitors (Pirtobrutinib) and emerging BTK degraders offer more selective inhibition, preserving T-cell function and potentially mitigating infection risk, though their long-term immunological impact requires further study. Infection susceptibility varies across BTK inhibitor generations, reflecting differences in kinase selectivity, modulation of humoral and cellular immunity, and disease-intrinsic immune dysfunction in chronic lymphocytic leukemia. This review examines the mechanistic basis of BTK inhibitor-associated immune dysfunction, compares generational differences in selectivity and safety profiles, and provides evidence-based recommendations for infection risk mitigation in clinical practice.

Endogenous retroviruses (ERVs), LINE-1 elements, and other endogenously active transposable-element families are now being studied for their role as a potential interface between epigenetic control and innate immunity. Here, we discuss how locus-specific failures in repressive complexes containing ATRX–DAXX–H3.3 and TRIM28–SETDB1–H3K9me3 may allow these elements to enter into unique molecular states that include double-stranded RNA, DNA/RNA hybrid molecules, RNA–protein complexes, reverse-transcription products, and RNA. Each of these states differs from the others in terms of its persistence, structural characteristics, and accessibility to sensors such as MDA5, RIG-I, cGAS–STING, and ZBP1, as well as host restriction pathways. We also emphasize that simply expressing a retroelement does not imply that it is competent to bind to a sensor and/or undergo productive retrotransposition. Rather, a distinction needs to be made between intermediate stages in the process of retrotransposition and productive retrotransposition itself. Therefore, the evidence needed to assign a specific sensor to a particular retroelement product must be presented. Furthermore, persistent stress caused by retroelement activity could converge with multiple cellular processes, such as p53–CDKN1A/p21-mediated cell-cycle arrest, PML-mediated nuclear organization, and lysosomal or metabolism-based changes leading to long-lived microglial states; however, demonstrating path dependence after removing the initiating perturbation would be required to demonstrate true hysteresis. Finally, downstream activation of complement pathways could have effects on synaptic function via separate CR3-dependent, trafficking-based, and contact-regulatory mechanisms. Overall, we recommend a locus-specific, structure-specific, and time-course-resolved approach for determining how the various states of endogenously active retroelements cross the genome–immunity boundary and contribute to neuroinflammatory dysfunction.