Background/Objectives: Differentiating between benign and malignant ovarian adnexal masses before surgery is a significant diagnostic challenge. This study examined a wide range of circulating plasma molecules (immune and inflammatory) to identify potential markers to classify tumors as benign or malignant. The goal was to develop a proof-of-concept tool for preoperative risk stratification. Methods: Twenty-three plasma molecules were evaluated in women with benign lesions (n = 68) and women with malignant ovarian tumors (n = 25). To evaluate the behavior of each marker in a normal population, women without adnexal pathology were also included (n = 11). The results were compared using the Kruskal–Wallis test with Dunn post hoc pairwise comparisons, the Benjamini–Hochberg correction for multiple comparisons, and ROC analysis. TGF-β isoforms and CA125 were measured in the complete cohort (n = 104), while the remaining molecules were assessed in a reduced cohort (n = 51). Two classification approaches were developed using TGF-β3 and IL-13: a sequential two-step algorithm and an ordinal logistic regression model. Apparent performance was corrected for optimism using Harrell’s bootstrap procedure. Results: Ten molecules reached statistical significance. Among the significant molecules, TGF-β3 identified ovarian lesions regardless of malignant status (AUC = 0.983), while IL-13 showed perfect malignancy-specific separation from benign cases (AUC = 1.000). Their combination in an ordinal logistic regression model produced three non-overlapping diagnostic strata across all three groups, significantly outperforming CA125, HE4, and ROMA at the malignancy-separation boundary (DeLong p < 0.05) in our exploratory cohort. Conclusions: TGF-β3 and IL-13 represent a biologically complementary marker pair whose combined ordinal regression model shows promising performance and warrants prospective validation in larger, multicenter independent cohorts as a preoperative risk-stratification tool for ovarian adnexal masses.

Hodgkin lymphoma (HL) is a common neoplasm in adolescents and young adults, primarily treated with doxorubicin (DOX) and bleomycin (BLM), which may cause severe adverse effects. The cure rate decreases to 75% in advanced-stage disease, highlighting the need for improved treatment strategies. Pentoxifylline (PTX), an NF-κB pathway inhibitor, enhances chemotherapy-induced apoptosis in cancer cells, making it a promising candidate for HL therapy. This study assessed the effects of PTX, DOX, and BLM on apoptosis, proliferation, and senescence in Hs-445 HL cells. Cell viability and clonogenicity were measured by spectrophotometry and spectrofluorimetry, while apoptosis, caspase activity, cell cycle, mitochondrial membrane potential (ΔΨm), proliferation, and senescence were analyzed via flow cytometry. Gene expression was assessed by qPCR. PTX significantly induced apoptosis, especially when combined with BLM or BLM+DOX (triple therapy), and modulated gene expression by upregulating proapoptotic and downregulating antiapoptotic markers. PTX increased caspase-3, -8, and -9 activity and disrupted the ΔΨm, particularly with BLM or triple therapy. Furthermore, PTX abolished DOX-induced G2 cell cycle arrest, reduced proliferation, and clonogenicity, and reversed DOX- and BLM-induced senescence. In conclusion, PTX induces apoptosis in HL cells, enhances DOX and BLM cytotoxicity synergistically, and reverses senescence, suggesting its potential as an adjunct therapy for HL.

Background/Objectives: Whether the COVID-19 pandemic uniformly increased antimicrobial resistance (AMR) is contested, and aggregate analyses may mask organism-specific patterns. The objective of the study was to characterize changes in the level and slope of monthly multidrug-resistant (MDR), possible extensively drug-resistant (pXDR), possible pandrug-resistant (pPDR), vancomycin-resistant enterococci (VRE), and methicillin-resistant Staphylococcus aureus (MRSA) positivity at a Mexican tertiary-care hospital, and to assess heterogeneity by organism, antimicrobial class, specimen type, and hospital service. Methods: Retrospective interrupted time-series of deduplicated bacterial isolates (October 2017 to January 2026), analyzed by segmented regression across pre-pandemic, pandemic, and post-peak phases. Results: Cohort-wide MDR positivity had been declining before 2020 and rose abruptly at pandemic onset (level shift +6.81 percentage points, p = 0.0092) with a simultaneous slope reversal, reaching 24.27 percentage points above the extrapolated pre-pandemic trend by February 2022 (95% CI 14.26–34.28, p < 0.0001). The decline resumed after the pandemic peak, but the two slope changes did not offset one another (joint p = 0.0064). pXDR and pPDR moved in the same direction (+8.93, p = 0.0233; +15.40, p = 0.0113). VRE showed no significant departure, whereas MRSA declined in every phase yet departed significantly from its extrapolated trajectory (+23.68, p = 0.0040). Among species, Escherichia coli showed the largest departure from its counterfactual (+48.82 percentage points, p < 0.0001) and Klebsiella pneumoniae had the largest abrupt level rise (+14.46 percentage points, p = 0.0055), while S. aureus declined in every phase despite an abrupt rise in level at pandemic onset. At the class level, carbapenem and third-/fourth-generation cephalosporin non-susceptibility rose at pandemic onset and returned to baseline afterwards (19.1% to 28.0% to 18.7%, and 51.7% to 59.4% to 52.5%; all q < 0.001), whereas fluoroquinolone non-susceptibility rose and did not revert, climbing further in E. coli (61.5% to 65.2% to 72.7%, q = 0.0012) and plateauing at an elevated level in K. pneumoniae (37.6% to 46.5% to 49.3%, q = 0.1919 post-peak). Conclusions: Resistance trajectories across pandemic-related phases were divergent and, for the Gram-negative organisms, incompletely reversed, with the highest burden of advanced resistance in high-intensity settings. Organism-resolved surveillance and sustained stewardship are needed.