
Pancreatic ductal adenocarcinoma (PDAC) exhibits oxidative stress adaptation and ferroptosis-associated transcriptional remodeling. We assessed redox- and ferroptosis-related expression scores using public transcriptomic cohorts and evaluated exploratory cross-cohort associations. The historical TCGA–GTEx tumor–normal comparison is potentially confounded by cohort origin and tissue collection, so its differential-expression findings are treated as descriptive rather than independently validated. In tumor-only analyses, the association between RedoxScore and FerroBalance differed between GSE15471 (Spearman ρ = −0.304, p = 0.0602) and GSE85916 (ρ = 0.243, p = 0.0299). In GSE85916, redox stratification was not associated with overall survival (log-rank p = 0.3313); the continuous Cox association was also non-significant (HR = 1.072, 95% CI 0.580–1.982; p = 0.8251). Four median-defined groups are therefore presented as descriptive quadrants, not validated molecular subtypes. These exploratory findings motivate further assessment using versioned gene sets, within-source comparisons, and molecular subtype annotations.
Drought is one of the most critical limiting factors in crop production. Our study investigated how salicylic acid (SA) pretreatment modified the subsequent drought stress response of tomato (Kecskeméti 549). Four groups (control, drought-stressed, SA-pretreated, and SA-pretreated and drought-stressed) were compared using genome-wide transcriptomic analyses based on RNA sequencing (n = 3) and antioxidant enzyme activity (peroxidase, catalase, glutathione reductase, glutathione-s-transferase, superoxide dismutase; POX, CAT, GR, GST, SOD). Chlorophyll content and biochemical factors such as proline, MDA, protein content, total phenols, total flavonoids and soluble sugars were also analyzed. Both SA treatment and drought stress caused extensive gene expression rearrangements, primarily in genes involved in redox homeostasis, signal transduction, proteostasis, and amino acid, carbohydrate, and energy metabolism. Under drought conditions, the transcriptional stress response of SA-pretreated plants was more moderate (with fewer chaperone, proteasome, defense, and redox genes being induced), while several SA-dependent WRKY factors (WRKY70, WRKY41, WRKY51, WRKY60) exhibited an induction response—contrary to the pattern observed in untreated plants. Furthermore, this group displayed the highest activity levels for all five antioxidant enzymes (two-way ANOVA, treatment × stress interaction). Transcript levels of the genes encoding these five antioxidant enzymes showed a strong correlation with their respective enzymatic activities (r = 0.85). Drought stress reduced leaf area by 24.6%, increased MDA content by 2.6 times, and reduced protein content by 79.3% in untreated plants. But in plants pretreated with SA, the leaf area did not decrease, the MDA content did not increase, and protein loss was lower (35.3%). These results indicate a persistent SA-induced priming effect.
Background/Objectives: The Q-Collar™, a device that mildly compresses the jugular veins to increase cranial fluid volume, has been investigated for potential protection against brain changes associated with concussive and subconcussive impacts during athletic events involving physical contact. However, physiological responses using this device as well as the physical and cognitive performance outcomes remain unclear. Therefore, the purpose of the study was to investigate hemodynamic, metabolic, prefrontal cortex oxygenation (PFC-O2Hb), choice reaction time (CRT) via the Stroop test, and time-to-completion outcomes with and without Q-Collar™ use. Methods: Eleven male participants qualified for inclusion into the repeated-measures randomized crossover study following an incremental cycling cardiopulmonary exercise test. Upon qualification, participants visited the lab twice to complete a 5 km cycling time trial with and without Q-Collar™ use. Each visit was separated by at least 72 h. Results: No statistically significant differences in hemodynamic, blood lactate (BLa−), PFC-O2Hb, or time-to-completion outcomes were found comparing Q-Collar™ use to a Control condition. However, improved CRT was found during, immediately following, and 10 min post the time trial relative to a resting CRT baseline. Conclusions: No statistically significant acute differences were detected between Q-Collar™ and Control for measured outcomes during a 5 km cycling time trial in this exploratory study. Smaller effects cannot be excluded, and because jugular compression was not verified during exercise, these findings reflect the effect of wearing a manufacturer-fitted Q-Collar™ rather than verified jugular compression. CRT was shorter during and after exercise relative to rest in both conditions, although repeated-testing effects cannot be excluded.
Oxidative stress contributes to acute myeloid leukemia (AML) biology and treatment resistance, but its prognostic relevance remains incompletely defined. We analyzed 553 patients from GSE37642, treating paired GPL96/GPL97 measurements from 417 patients as the discovery cohort and GPL570 (n = 136) as a platform-defined internal–external validation cohort. Human genes annotated to cellular response to oxidative stress (GO:0034599) were retrieved from the Enrich GO Biological Process 2023 library; 110 genes were measurable in both cohort definitions. Discovery-only preprocessing was frozen before validation. Seventeen genes with nominal univariate Cox p < 0.05 entered cross-validated LASSO–Cox modeling, which retained a 13-gene signature (ATP13A2, AKT1, DAPK1, HSPA1A, LRRK2, CPEB2, CAMKK2, CCS, PRKAA1, RBM11, TP53, GPX1, and TPM1). Using the fixed discovery-derived coefficients and median cutoff (0.00807), the score separated high- and low-risk patients in discovery (log-rank p = 3.51 × 10−12; continuous-score HR = 3.24, 95% CI 2.46–4.29; C-index = 0.627, 95% CI 0.591–0.661) and remained associated with survival in platform-defined validation (log-rank p = 0.019; HR = 1.90, 95% CI 1.20–3.00; C-index = 0.580, 95% CI 0.519–0.641). Validation AUCs were 0.590, 0.621, and 0.655 at 1, 3, and 5 years. A fully nested five-fold diagnostic yielded a mean held-out C-index of 0.571. Adding the risk score to age improved the nested-model fit in validation (likelihood-ratio p = 0.028), but the improvement in discrimination was small (Delta C-index = 0.019) and its paired out-of-bag bootstrap 95% CI included zero (−0.070 to 0.056); corresponding Delta AUC intervals also included zero. Schoenfeld diagnostics did not indicate proportional-hazards violations. These findings support a biologically interpretable oxidative-stress-associated prognostic signal with modest cross-platform discrimination, while emphasizing the need for independent contemporary validation before clinical use.
Although dioxygen is indispensable for aerobic metabolism and cellular energy production, excessive exposure to oxygen can induce oxidative damage, thereby accelerating cellular dysfunction, promoting disease progression, and contributing to aging—a phenomenon commonly referred to as “oxygen toxicity.” To date, no experimental or theoretical studies have, to the best of our knowledge, examined the capture of triplet-ground-state O2 by stable triplet-ground-state molecular species. The present study therefore introduces a novel conceptual approach to the activation and capture of triplet O2. Thermodynamic and kinetic analyses reveal that, among the Group 15 pnictinidenes investigated, only [P-Rea]3 and [As-Rea]3 exhibit thermodynamically and kinetically favorable O2-capture processes. Activation strain analysis further demonstrates that the activation barrier is governed predominantly by the deformation energy required to distort the O2 molecule, together with the influence of the atomic radius of the Group 15 center.