Citations

The primary aim of this study was to examine pitching performance metrics before and after ulnar collateral ligament reconstruction (UCLR) among Major League Baseball (MLB) starting and relief pitchers. The following information was extracted from the “Tommy John Surgery List” database regarding UCLR surgeries among MLB pitchers: UCLR date, pitcher type (starting pitcher, relief pitcher), and age at time of UCLR. Pitching performance metrics were extracted from the Baseball Savant online platform for the two seasons immediately prior to UCLR (pre) and the two seasons immediately following returning to pitching after UCLR (post). Fifty-nine pitchers were included in this study (29 starting pitchers, 30 relief pitchers). The outcome measures included the number of pitches thrown, earned run average (ERA), walks plus hits per inning pitched (WHIP), strikeout percentage, whiff percentage, walk percentage, batting average against, ground ball percentage, and fastball velocity. There was a pitcher type-by-time interaction effect for ERA (p = 0.01; η2 = 0.12) and WHIP (p = 0.01; η2 = 0.12). Starting pitcher ERA increased from 3.68 to 4.40 from pre- to post-surgery, while relief pitcher ERA decreased from 4.47 to 3.90. In addition, starting pitcher WHIP increased from 1.22 to 1.29 from pre- to post-surgery, while relief pitcher WHIP decreased from 1.38 to 1.28. There was a main effect of time for pitches thrown (p = 0.04; η2 = 0.07). Significant differences between starting and relief pitchers were observed for changes in ERA and WHIP following UCLR, whereas no pitcher type-by-time interactions were observed for the remaining performance metrics. Both starting and relief pitchers threw fewer pitches following UCLR, while fastball velocity and other key pitching performance metrics remained largely unchanged.

Abstract Horlock, CF, Allen, LE, Jagim, AR, Jones, MT, and Fields, JB. In-season assessment of dietary intake and match demands of men’s collegiate Rugby Sevens players. J Strength Cond Res XX(X): 000–000, 2026—Limited research has examined the external workload demands and dietary intake of collegiate men's Rugby Sevens players. Therefore, the purpose of this study was to (a) quantify match demands in Division 1-AA collegiate Rugby Sevens across a competitive season, and (b) assess players' dietary intake relative to sport-specific nutrition guidelines. Division 1-AA men's collegiate Rugby Sevens players ( n = 13; age: mass: 87 ± 14 kg; body fat %: 20 ± 4%) wore a global positional system device during all matches ( n = 17). External load metrics were total distance (TD) (m), sprint distance (>20.1 km·h −1 ), high-intensity distance (>18.1–20.0 km·h −1 ), meters per minute (m·min −1 ), acceleration efforts (#), deceleration efforts (#), sprint efforts (#), high-speed efforts (#), player load (PL) (arbitrary unit [AU]), PL per minute (AU/min), and estimated energy expenditure (EE) (kcal). Dietary intake was assessed at the start of the season using a 4-day food log. Linear mixed models examined changes in workload parameters across tournament matches. Spearman's rank correlation and linear regression assessed relationships and predictability of EE and external workloads. One-samples t test compared dietary intake relative to established guidelines ( p ≤ 0.05). No significant differences in workload metrics were observed across individual matches. Total distance ( r = 0.968, p < 0.001), m·min −1 ( r = 0.973, p < 0.001), PL ( r = 0.912, p < 0.001), and PL/min ( r = 0.855, p < 0.001) had the strongest correlations with EE. Players significantly underconsumed calories ( p = 0.028) and carbohydrates ( p < 0.01). Monitoring external workloads and assessing dietary intake can provide coaches with strategies to optimize sports performance and nutrition support to prepare players for competition demands.

Introduction Female distance runners are at elevated risk for impaired bone remodeling due to high mechanical loading, potential low energy availability, and sustained inflammatory stress. Collagen peptide (CP) supplementation has been proposed as a nutritional strategy to support type I collagen synthesis and modulate osteoimmune signaling; however, evidence in premenopausal endurance athletes is limited. This pilot randomized, double-blind, placebo-controlled trial examined the effects of four weeks of high-dose CP supplementation on markers of bone metabolism and inflammatory activity in endurance-trained premenopausal women. Methods Twenty-two participants (18–35 years; ≥35 miles/week [&gt;56km/week]) were randomized to CP (INT; 20 g/day) or isocaloric maltodextrin (CON). Pre- and post-intervention assessments, conducted in the early follicular phase, included serum procollagen type I N-terminal propeptide (P1NP), plasma C-terminal telopeptide of type I collagen (CTX-1), serum soluble receptor activator of nuclear factor-κB ligand (sRANKL), osteoprotegerin (OPG), the sRANKL/OPG ratio, and interleukin-6 (IL-6). Repeated-measures ANCOVAs were performed, adjusting for accumulated running distance and vitamin D status. Results A significant group × time interaction was observed for P1NP ( p = 0.04), with increases in INT and no change in CON. No significant interaction was observed for CTX-1 ( p = 0.13). Significant interactions were also observed for sRANKL ( p = 0.046) and IL-6 ( p = 0.03). No significant interaction effects were detected for sRANKL, OPG, or the sRANKL/OPG ratio. Discussion Short-term CP supplementation increased a marker of bone formation, altered osteoclast-related signaling, and reduced IL-6 in endurance-trained premenopausal women. These findings support the potential for CP-mediated modulation of bone turnover and inflammatory activity and warrant further investigation in larger, adequately powered trials incorporating structural bone outcomes.

Tumor Treating Fields (TTFields) represent a novel, non-invasive therapeutic modality in oncology that employs low-intensity, intermediate-frequency alternating electric fields to disrupt mitotic processes and induce cancer cell death. This review integrates mechanistic, preclinical, and emerging clinical evidence supporting the integration of TTFields with immunotherapeutic strategies in pancreatic ductal adenocarcinoma (PDAC). Although immunotherapy has transformed the treatment landscape across multiple malignancies, its efficacy in PDAC remains limited due to the tumor’s dense stroma, immunosuppressive microenvironment, and low immunogenicity. Preclinical investigations suggest that TTFields may potentiate immune-based therapies by enhancing antigen presentation, modulating the tumor microenvironment (TME), and attenuating mechanisms of immune resistance. We highlight studies evaluating TTFields in combination with immune checkpoint inhibitors (ICI), adoptive cellular therapies, and cancer vaccines, emphasizing their potential synergistic effects in PDAC. Clinically, the phase II PANOVA-2 trial demonstrated feasibility and encouraging survival outcomes with TTFields in combination with gemcitabine and nab-paclitaxel, providing the rationale for the ongoing phase III PANOVA-3 trial and the phase II PANOVA-4 trial, which combines TTFields with chemotherapy and atezolizumab. Additional clinical experiences in glioblastoma (GBM) and non-small-cell lung cancer (NSCLC) further substantiate the broader applicability of TTFields as an immunomodulatory adjunct. Remaining challenges include optimizing treatment sequencing, identifying predictive biomarkers, and managing TTFields-associated toxicities. Collectively, current evidence positions TTFields as a promising strategy to augment immunotherapy in PDAC, warranting further translational and clinical investigation to establish its role in reshaping therapeutic paradigms.

Abstract Alzheimer’s disease (AD) emerges from multi-scale interactions between molecular pathology and disruptions in large-scale brain network dynamics. Understanding how these processes co-evolve and relate to disease stages is essential for advancing complex systems models of aging and AD, and for developing system-informed interventions. However, progress has been limited by a lack of large-scale longitudinal data. To address this, we examined the longitudinal relationship between subsystems of the default mode network (DMN) (posterior DMN, ventral DMN, anterior dorsal DMN) using task-free functional MRI (fMRI) and amyloid positron emission tomography (PET) imaging in a large longitudinal cohort spanning the clinico-biological spectrum of AD (n = 1,451; 2,763 time points) using mixed-effect models. We also assessed whether patterns of DMN connectivity predicted conversion to amyloid positivity, mild cognitive impairment (MCI), and dementia using Cox proportional hazards models. Our findings reveal a dynamic interplay between amyloid accumulation and connectivity within and between DMN subsystems, with both hyper- and hypoconnectivity emerging across DMN subsystems in association with increasing amyloid burden. Importantly, survival models showed that DMN connectivity patterns predicted conversion to critical stages of the disease, including not only conversion to MCI and dementia, but also conversion to amyloid positivity in otherwise clinically unimpaired individuals who were amyloid negative at baseline. These associations were independent of age, APOE4 status, sex, education, and in-scanner motion. These results support a model in which breakdowns in tightly regulated feedback loops governing DMN physiology represent a core systems-level pathophysiology of AD. Notably, this functional dyshomeostasis precedes detectable amyloidosis on imaging. Future studies should focus on the development of robust biomarkers of brain function that can be applied at the individual level, which could in turn help support the development of therapeutic approaches targeting system-level pathophysiology.

Abstract Background: Pancreatic ductal adenocarcinoma (PDAC) remains highly lethal due to aggressive biology, stromal desmoplasia, and profound immunotherapy resistance. Tumor Treating Fields (TTFields) disrupt mitosis and induce immunogenic cell death (ICD), type I interferon signaling, and microenvironment remodeling, providing a rationale for combining TTFields with immune checkpoint inhibition. This is the first systematic review to comprehensively synthesize mechanistic and clinical evidence for TTFields immunotherapy combinations across solid tumors, with emphasis on their translation relevance to PDAC. Methods: A systematic search of PubMed, Scopus, Web of Science, Embase, Cochrane Library, and ClinicalTrials.gov was conducted through October 26, 2025, following PRISMA 2020 guidelines. Eligible studies evaluated TTFields combined with immunotherapy. Two reviewers independently screened and extracted data using Covidence. Evidence was summarized narratively by tumor type, study design, and immunotherapeutic approach. Results: Thirty-seven studies met criteria, including preclinical and clinical investigations across glioblastoma, NSCLC, mesothelioma, PDAC, and other tumors. Preclinical models consistently showed that TTFields trigger ICD hallmarks such as calreticulin exposure, HMGB1 and ATP release, and activate STING/type I interferon pathways, enhancing dendritic-cell maturation and T-cell and NK-cell function. Across in vivo models, TTFields combined with PD-1 or CTLA-4 blockade, vaccines, or other immunotherapies reduced tumor growth and increased lymphocyte infiltration. Clinical evidence, although early-phase and heterogeneous, indicates the combination is feasible, with toxicity dominated by low-grade skin reactions and no excess immune-related adverse events. In glioblastoma, adding TTFields to pembrolizumab and temozolomide showed numerically improved survival. The LUNAR phase 3 trial in metastatic NSCLC demonstrated an overall survival advantage when TTFields were added to systemic therapy, including immunotherapy. Evidence in PDAC remains preliminary, but the ongoing PANOVA-4 study combining TTFields with atezolizumab and chemotherapy highlights emerging translational relevance. Conclusions: TTFields enhance antitumor immunity when combined with immunotherapy across solid tumors. In PDAC, these mechanisms may help counteract the immunosuppressive microenvironment. Ongoing gastrointestinal trials will clarify optimal combinations, biomarkers of response, and the clinical role of TTFields-based immunomodulation. Citation Format: Douaa Albelal, Hari Krishnareddy Rachamala, Hani Babiker. Synergistic immunomodulation by Tumor Treating Fields combined with immunotherapy across solid tumors: A systematic review with translational relevance to pancreatic ductal adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 3813.