Search Results (4,262)

Background/Objectives: Androgenetic alopecia (AGA) responds only partially to pharmacologic monotherapy. Combination procedural regimens incorporating platelet-rich plasma (PRP), stromal vascular fraction (SVF), and botulinum toxin (BTX) have been reported, but objective quantitative trichoscopic data on multimodal single-session protocols are limited. We retrospectively quantified the trichoscopic response to a four-component single-session scalp procedure used in routine clinical practice. Methods: Fifty-one consecutive AGA patients underwent a single-session procedure combining partial temporalis muscle resection with silicone implantation, negative-pressure scalp stimulation, and BTX, PRP, and SVF injections; 28 completed ≥ 4-month follow-up. Standardized 60× videodermoscopy at five predefined scalp locations was archived for paired quantitative analysis in six patients (30 location pairs, of which 28 were analyzable after excluding two pairs for motion artifact), with one additional patient imaged at four years. Six trichoscopic outcomes were derived by automated image analysis (Otsu thresholding, skeletonization, distance-transform shaft thickness); the primary analysis was performed at the patient level (n = 6) and a supporting analysis at the panel level (n = 28), each using paired Student’s t-tests. Results: In the primary patient-level analysis (n = 6 patients), five of six trichoscopic outcomes improved significantly at 3–4-month follow-up, each with a large effect size: median shaft thickness +54% (p = 0.025), terminal-hair proportion +52% (p = 0.028), vellus-hair proportion −33% (p = 0.011), diameter heterogeneity −14% (p = 0.017), and mean shaft thickness +33% (p = 0.029); hair coverage increased but did not reach statistical significance (+11%, p = 0.125). The supporting panel-level analysis (n = 28 paired panels) was concordant in direction and significant for all six metrics. In a single illustrative case followed for four years (n = 1; exploratory), mean shaft thickness gain (+41%, p = 0.039) and vellus reduction (−36%, p = 0.025) were sustained, while the transient coverage gain at 3–4 months (+38%, p = 0.007) partially receded. Conclusions: In this preliminary case series, the integrative procedure was associated with quantifiable trichoscopic re-thickening rather than gross densification, with sustained shaft-caliber gain at four years in the long-term case. Causal attribution to any single component is not possible from this single-arm design; prospective controlled trials are required. Full article

Periprosthetic joint infection (PJI) remains a major clinical challenge after total joint arthroplasty because of its association with prolonged antimicrobial therapy, repeated surgery, implant failure, functional disability, and substantial socioeconomic burden. Current strategies, including systemic antibiotics, debridement with implant retention, staged revision, and antibiotic-loaded cement spacers, remain indispensable but are limited by mature biofilm tolerance, protected microbial reservoirs, insufficient local drug penetration, persistent inflammation, and compromised periprosthetic bone repair. Increasing evidence indicates that PJI is not merely bacterial colonization of an implant surface, but a dynamic prosthetic interface disorder involving biofilm persistence, immune dysregulation, inflammatory osteolysis, and failed osseointegration. This review summarizes recent advances in anti-infective prosthetic interface design, emphasizing the transition from passive antibacterial coatings toward multifunctional immuno-antibacterial osseointegrative systems. The pathogenic basis of PJI is first discussed, including conditioning film formation, bacterial adhesion, biofilm maturation, protected reservoirs, immune evasion, and osteolysis. Current clinical management limitations are then evaluated, followed by emerging biomaterial strategies, including anti-adhesive and contact-killing surfaces, active antimicrobial coatings, mature biofilm disruption, biological antibiofilm therapies, smart infection-responsive delivery systems, and osteoimmunomodulatory interfaces. Particular attention is given to balancing early antibacterial activity with cytocompatibility, immune resolution, angiogenesis, mechanical durability, and long-term osseointegration. Finally, key translational barriers are highlighted, including load-bearing and tribological constraints, insufficiently standardized mature biofilm and animal models, limited clinical evidence for advanced smart materials, manufacturing reproducibility, sterilization compatibility, regulatory complexity, and application-specific clinical readiness. Future anti-PJI interfaces should evolve beyond unidirectional bacterial killing toward stage-specific systems integrating biofilm control, immune restoration, vascularized bone regeneration, and durable mechanical performance. Full article

Background/Objectives: Herpesviridae have been increasingly investigated as possible contributors to Alzheimer’s disease (AD) because of their neurotropism, lifelong latency, and capacity to modulate inflammatory and amyloid-related pathways Methods: This structured narrative review, based on a systematic literature search, examined original studies published between December 2020 and December 2025 on the association between human herpesviridae and AD. Searches were conducted in PubMed, Web of Science, and Scopus using a PRISMA-informed screening framework. Results: The available evidence was heterogeneous across viruses and study designs. HSV-1 emerged as the most consistently implicated virus, supported by epidemiological, biomarker, neuroimaging, and experimental studies, although contradictory findings were also reported. VZV was mainly associated with AD through vascular, inflammatory, and vaccination-related evidence, with several studies suggesting lower dementia risk after zoster vaccination. CMV, EBV, and HHV-6 showed biologically plausible but less consistent associations, whereas HHV-7 and HHV-8 were supported only by limited or indirect evidence. Across studies, the proposed mechanisms included chronic neuroinflammation, vascular injury, amyloid and tau dysregulation, host immune responses, and cumulative infectious burden. Conclusions: Overall, the literature suggests that the relationship between herpesviridae and AD is not uniform and that HSV-1 appears to be the most relevant candidate. However, methodological heterogeneity, possible reverse causation, and unequal study intensity across viruses limit firm conclusions. More robust longitudinal and subtype-specific studies are needed to clarify causal relevance. Full article

Background: Hypertension-induced vascular injury involves endothelial dysfunction, inflammation, and oxidative stress, leading to vascular remodeling and cardiovascular complications. Flavin-containing monooxygenase 2 (FMO2) has been implicated in redox regulation, but its role in hypertensive vascular injury remains unclear. This study investigated whether KuJiang GanLuoYin (KJGLY) protects against hypertensive vascular injury and whether FMO2-associated Fat mass and obesity-associated protein (FTO)/N6-methyladenosine (m⁶A) signaling is involved. Methods: Spontaneously hypertensive rats (SHRs) were treated with KJGLY for eight weeks. Blood pressure, vascular remodeling, inflammation, oxidative stress, and global m⁶A RNA methylation were assessed. Integrated metabolomic and proteomic analyses were performed to identify treatment-associated molecular alterations and candidate proteins. AAV9-mediated FMO2 knockdown in SHRs and gain- and loss-of-function approaches in angiotensin II (Ang II)-stimulated human umbilical vein endothelial cells were used to examine the functional involvement of FMO2. Ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS)-based chemical profiling and High-performance liquid chromatography–tandem mass spectrometry (HPLC–MS/MS) quantification were performed to characterize the major constituents of KJGLY. Results: KJGLY significantly reduced blood pressure and alleviated vascular remodeling in SHRs. Metabolomic and proteomic analyses revealed treatment-associated alterations in inflammatory and lipid metabolic pathways and identified FMO2 as a treatment-responsive candidate. KJGLY restored FMO2 expression, reduced FTO abundance and NF-κB activation, increased global m⁶A levels, and attenuated inflammatory and oxidative stress responses in hypertensive aortas. Conversely, AAV9-mediated FMO2 knockdown aggravated vascular injury, enhanced inflammation and oxidative stress, reduced global m⁶A levels, and increased NF-κB activation. Co-immunoprecipitation showed an association between FMO2 and FTO, and MeRIP-qPCR indicated that FMO2 manipulation altered m⁶A enrichment of VCAM-1 mRNA. In Ang II-stimulated endothelial cells, linarin, the most abundant quantified constituent of KJGLY, partially recapitulated the cellular effects of KJGLY, including restoration of FMO2/FTO-associated signaling and attenuation of inflammatory activation. Conclusions: These findings support a functional role for FMO2 in hypertensive vascular injury and suggest that FMO2-associated modulation of FTO/m⁶A signaling may contribute to the vascular protective effects of KJGLY. Linarin recapitulated key protective effects in vitro, although its in vivo contribution to the formula remains to be determined. Full article

Radiotherapy-associated pain is among the most common and debilitating complications in head and neck cancer. Although historically viewed primarily as a treatment-related adverse effect, growing evidence suggests that pain is deeply intertwined with tumor biology, immune remodeling, and therapeutic outcomes. At the same time, recent advances in cancer neuroscience have identified sensory nerves as active components of the tumor microenvironment (TME), capable of influencing antitumor immunity through complex neuroimmune crosstalk. These observations raise the possibility that radiotherapy-associated pain is not merely a clinical symptom but also a biological indicator of dynamic changes within the tumor immune microenvironment (TIME). In this review, we outline the major clinical manifestations of radiotherapy-associated pain in head and neck cancer, including inflammatory or mucositis-related pain, neuropathic pain, and long-term chronic pain, with emphasis on their underlying biological features and potential therapeutic relevance. Given that oral mucositis is the dominant source of acute radiotherapy-associated pain in head and neck cancer, we further summarize evidence-based preventive and supportive strategies, including photobiomodulation, mucosal barrier-forming agents, anti-inflammatory mouthwashes, nutritional interventions, pain control, and multidisciplinary oral care. We further discuss how radiotherapy reshapes the TIME through mechanisms such as immunogenic cell death, activation of the cGAS-STING pathway, vascular and stromal remodeling, and regulation of lymphoid compartments, while also triggering compensatory immunosuppressive responses. Preclinical and translational studies suggest that nociceptive signaling pathways may modulate T-cell function, myeloid-cell activity, and immune-evasive programs. Through these neuroimmune interactions, radiotherapy-induced neural injury and persistent pain may contribute to the establishment of an immunosuppressive, wound-like microenvironment that ultimately affects treatment response and tumor progression. Finally, we discuss the translational significance of incorporating pain phenotyping into combined radiotherapy and immunotherapy strategies for head and neck cancer. Opioid-sparing multimodal analgesia, neuromodulation, and neuroimmune-targeted interventions may represent promising approaches to simultaneously improve symptom control and antitumor immunity. We propose that radiotherapy-associated pain may be considered a candidate neuroimmune phenotype rather than a passive adverse event, providing a new conceptual framework for precision management and translational research in head and neck cancer. Full article

Coronary drug-eluting stents (DESs) are the current clinical standard, yet delayed endothelialization remains a critical challenge. Graphene-based coatings have emerged as promising cardiovascular biomaterials due to their favorable hemocompatibility and ability to support endothelial cell growth. In this study, we evaluated the in vivo performance of graphene-coated stents (GCSs) compared with commercial sirolimus-eluting stents in a Polish White swine model (n = 10). Stents were implanted into major coronary branches, with follow-up at 30 and 90 days using quantitative coronary angiography (QCA), optical coherence tomography (OCT), and cryogenic scanning electron microscopy (cryo-SEM). No systemic toxicity, mortality, thrombotic events, or ischemic complications were observed during the study period. QCA demonstrated no significant differences in percent diameter stenosis between GCSs and DESs at either 30 days (12.3 ± 6.1% vs. 8.6 ± 5.8%, p = 0.2782) or 90 days (18.3 ± 10.5% vs. 9.6 ± 6.6%, p = 0.1074). OCT analysis confirmed comparable lumen and neointimal parameters between groups, while demonstrating a favorable, although non-significant, trend toward a lower percentage of uncovered struts in GCSs. Cryo-SEM imaging demonstrated stable tissue integration and a preserved healing response surrounding GCSs. Collectively, these findings indicate that GCSs are safe and biocompatible and demonstrate mid-term vascular performance comparable to clinically used DES platforms. The presented results support further investigation of graphene-based coatings as potential surface-modification strategies for coronary stents. Full article

Bone regeneration is governed by a tightly coordinated interplay between skeletal cells, immune cells, vascular components, and signaling networks within a dynamic microenvironment. Increasing evidence from osteoimmunology demonstrates that immune regulation is not merely supportive but mechanistically determinative of regenerative outcomes. Dysregulated or persistent inflammation can impair osteogenesis, whereas timely immune resolution promotes angiogenesis and matrix deposition. In this context, nanotechnology has enabled the development of nanoparticles (NPs) that function not only as delivery vehicles but also as active modulators of the bone immune microenvironment. Immunomodulatory NPs can be engineered to deliver bioactive agents, regulate cytokine networks, and influence immune cell phenotypes, particularly macrophage polarization, at defined stages of healing. Through tailored surface chemistry, targeting ligands, and stimuli-responsive release mechanisms, NPs can achieve spatially localized and temporally controlled modulation of inflammatory and reparative phases, thereby enhancing osteogenesis and vascular integration. This review provides a comprehensive overview of organic, inorganic, and hybrid NP platforms applied to bone regeneration, with emphasis on their mechanisms of immune modulation, strategies for cell-specific targeting, and approaches for sequential regulation of inflammatory resolution and tissue repair. By integrating advances in materials science and immunology, NP-enabled platforms have the potential to transform bone regeneration from passive structural repair into precision immune-guided healing. Full article

Background/Objectives: Migraine is a common neurovascular disorder associated with substantial disability. Increasing evidence suggests that hypoxia-related signaling, endothelial dysfunction, and nitric oxide metabolism contribute to its pathophysiology. This study investigated the relationships between hypoxia-inducible factor-1 alpha (HIF-1α), vascular endothelial growth factor A (VEGF-A), and arginine pathway metabolites in chronic migraine. Methods: In this observational study, fasting ethylenediaminetetraacetic acid (EDTA) plasma samples were obtained from 28 patients with chronic migraine and 28 healthy controls. Arginine, citrulline, and ornithine concentrations were quantified by liquid chromatography–tandem mass spectrometry, whereas HIF-1α and VEGF-A were measured using enzyme-linked immunosorbent assays. Group comparisons, receiver operating characteristic analyses, and Firth penalized logistic regression models were performed. Results: Patients with chronic migraine exhibited significantly higher VEGF-A and HIF-1α concentrations than controls (both FDR-adjusted p ≤ 0.001). VEGF-A demonstrated excellent discrimination of migraine status (AUC = 0.973), whereas HIF-1α showed good discriminatory performance (AUC = 0.794). The arginine-to-citrulline ratio was higher (FDR-adjusted p = 0.032) and ornithine concentrations were lower (FDR-adjusted p = 0.043) in migraine patients. In multivariable analyses, VEGF-A (OR = 14.46), HIF-1α (OR = 5.83), and ornithine (OR = 0.28) remained independently associated with migraine status. Conclusions: Chronic migraine was associated with elevated circulating HIF-1α and VEGF-A concentrations together with alterations in arginine metabolism. These exploratory findings suggest that hypoxia-responsive signaling, endothelial activation, and nitric oxide-related metabolic pathways may represent interconnected biological processes associated with chronic migraine. Larger longitudinal and externally validated studies are required to confirm these observations and clarify their potential clinical relevance. Full article

Endothelial VEGFR-2 plays a central role in vascular remodeling during intestinal inflammation, yet its activation during the early stages of colitis remains poorly characterized. Because Akt is a major downstream effector of VEGFR-2 signaling and a key mediator of endothelial responses, we investigated whether VEGFR-2 phosphorylation and Akt activation occur during the early phase of TNBS-induced colitis before the development of extensive mucosal injury. Acute colitis was induced in adult female Wistar rats by intracolonic administration of TNBS. Colonic tissues were collected on days 2, 4, and 6 after induction. Histological analyses and macrophage (CD68⁺ cells) infiltration were performed to characterize disease progression. VEGFR-2 expression and phosphorylation at Tyr1175 were evaluated on day 4 by Western blot, immunoprecipitation, and immunofluorescence. Akt activation was also assessed. TNBS-induced colitis is characterized by histological injury and increased CD68⁺ macrophage infiltration on day 4, with severe tissue damage observed on day 6. On day 4, colitis is associated with increased endothelial VEGFR-2 expression, enhanced VEGFR-2 phosphorylation at Tyr1175, and Akt activation. Early TNBS-induced colitis is associated with endothelial VEGFR-2 phosphorylation and Akt activation before the onset of extensive mucosal destruction on day 6. These findings support activation of the VEGFR-2/Akt signaling axis as an early vascular response during intestinal inflammation and suggest its potential contribution to disease progression. Full article

Background: During life, all organisms experience multiple stressful events capable of disrupting their somatic integrity. As mammals, humans respond to environmental, sociocultural, and cognitive stressors via allostasis, a systemic neurophysiological response that supports physiological homeostasis. Unfortunately, allostatic mechanisms are incapable of countering all stressors, and systemic physiological damage accumulates with age; thereby contributing to physiological dysregulation and an increasing allostatic load (AL). Previously, we reported that a ten-factor allostatic load index (ALI) varied significantly by age, gender, and rural–urban residence in a sample of Polish citizens ages 55+ years but a five-biomarker frailty index did not. Here we determine whether an estimated ALI covaries with self-reported food intakes across age, residential setting, and gender. Methods: Two hundred and ten residents of Greater Poland ages 55–91 years, residing in either the Nekla commune (N = 103) or the capital of Greater Poland, Poznan (N = 107), participated in research designed to estimate a study-specific 10-biomarker ALI and its possible associations with their self-reported dietary choices, age, gender, and residential location. Of these, 206 completed study protocols including a food frequency questionnaire, verifying their age, self-reporting their gender, and allowing research personnel to obtain data for assessing 10 physiological biomarkers of allostatic load for inclusion in a study-specific ALI. Statistical significance for nominal measures was estimated using chi-square analyses; those for continuous measures, t-tests. Results: In the full sample, self-reported higher red meat and snack intakes were significantly associated with higher ALI at younger ages (55–69 years). No food item was significantly associated with estimated ALI at older ages (70+ years). Further, low self-reported intakes of fish and seafood consumption were significantly associated with a higher ALI in Poznan, but not Nekla residents. Within the full sample, average ALI was almost identical between younger and older women. Conclusions: In this cross-sectional sample of older Nekla and Poznan residents allostatic load not only varied by age, sex, and residential location, but also with self-reported consumption of red meat, snacks, fish and seafood. Observed differences in biomarkers of AL between younger and older residents of Poland across this sample suggest possible higher incidences of chronic disease occur among women residing in Nekla than those in Poznan. Similarly, the significant associations of red meat and snack consumption with ALI at younger ages in both settings may portend increasing vascular disease and related complications among those ages 55–69 years in this sample as they age. As does the higher estimated ALI among Poznan residents reporting low fish and seafood consumption. Full article

The periorbital region represents one of the most challenging anatomical sites in aesthetic medicine due to its thin dermis, complex vascularity, and susceptibility to oedema and contour irregularities. While hyaluronic acid (HA) fillers remain the gold standard for volumetric correction, their limitations in skin quality enhancement and risk of complications such as Tyndall effect and malar oedema have driven interest in regenerative alternatives. Polynucleotides (PN), particularly polydeoxyribonucleotides (PDRN), have emerged as bioactive agents capable of promoting dermal remodelling, angiogenesis, and anti-inflammatory responses. This review critically evaluates current evidence comparing PN and HA in periorbital rejuvenation, integrating mechanistic insights, clinical outcomes, and safety considerations. While HA remains superior for structural correction, PN demonstrates consistent improvements in dermal quality parameters, including elasticity, hydration, and fine rhytids, with a favourable safety profile. However, heterogeneity in study design, product formulation, and outcome measures limits the ability to draw definitive conclusions. Future research should prioritise standardised protocols, long-term follow-up, and direct comparative trials to establish optimal treatment algorithms. Full article

Objective: To determine whether contrast therapy improves recovery after climbing-specific forearm fatigue in amateur climbers. Methods: In a randomized repeated-measures trial, 40 climbers were allocated to passive recovery (n = 20) or Game Ready contrast therapy (n = 20). Both groups completed a fixed-task intermittent fingerboard protocol on a 20 mm edge using a half-crimp grip, with 7 s of work and 3 s of rest for five sets; the load was not individualized to climbing-specific maximal finger-flexor force. The intervention group received bilateral forearm treatment consisting of alternating 1 min cold (3 °C) and heat (45 °C) phases combined with pneumatic compression ranging from 15 to 75 mmHg. Sessions lasted 20 min and were administered immediately after post-fatigue testing, at 24 h and 48 h, and then three times weekly on alternate days for 8 weeks, for a total of 27 sessions. Outcomes were assessed at baseline, immediately after fatigue, at 24 h and 48 h, and after 8 weeks. Outcomes included perfusion, reactive hyperemia, stiffness, pressure pain threshold, grip strength, perceived recovery, creatine kinase, and interleukin-6. Results: Immediate post-fatigue responses were comparable. Contrast therapy produced greater 24 h and 48 h resting perfusion responses (+7.28 percentage points, 95% CI 6.58 to 7.98; +7.62, 95% CI 6.94 to 8.31; both adjusted p < 0.001). At week 8, peak hyperemic perfusion improved more with contrast therapy (+6.21 PU, 95% CI 5.62 to 6.79; p < 0.001). Recovery favored contrast therapy for stiffness at 48 h (−71.7 N/m, 95% CI −75.6 to −67.8), pressure pain threshold at week 8 (+8.1 N/cm², 95% CI 7.3 to 8.8), and grip strength at 48 h (+7.8 kgf, 95% CI 7.3 to 8.3; all p < 0.001). CK and IL-6 differences were transient, and no serious adverse events or intervention-related discontinuations were recorded. Conclusions: Contrast therapy was associated with more favorable cutaneous perfusion, post-occlusive reactive hyperemia-derived, and neuromechanical recovery outcomes, whereas biochemical differences were limited and time-dependent. The vascular findings do not establish improved endothelial function or nitric-oxide-mediated vasodilation because these mechanisms were not directly assessed. Trial registration: ISRCTN49499065 on 23 June 2025. Full article

Dravet syndrome (DS) is a severe developmental and epileptic encephalopathy caused by SCN1A haploinsufficiency. While brain pathology has been extensively studied, the retina remains underexplored. This study investigated retinal structural, functional, vascular, and cellular changes in a Scn1a^+/− rat model of DS. Anatomical quantification revealed thinning of the retinal nerve fiber layer and thickening of the outer plexiform layer. Electroretinography (ERG) showed selectively reduced oscillatory potential amplitudes, suggesting dysfunction of neurovascular coupling. Consistent with these findings, immunohistochemistry demonstrated aberrant vascular morphology, including increased vessel curvature and reduced branching density. In addition, we observed robust microglial activation in the outer and inner plexiform layers; however, astrocyte morphology remained largely unchanged. Fenfluramine, an approved anti-seizure drug for DS, attenuated microglial activation but failed to rescue retinal structural or vascular deficits, indicating a dissociation between its anti-inflammatory and disease-modifying effects. Our findings suggest that multimodal retinal assessment could serve as a noninvasive biomarker platform for monitoring disease progression and therapeutic response in DS. Full article

Background/Objectives: It is unclear if adherence to healthy guidelines can modify the association between polygenic risk score (PRS) for type 2 diabetes and dementia. This study aimed to investigate interrelationships between PRS for type 2 diabetes, Life’s Essential 8 (LE8) metrics, and dementia. Methods: We included 437,732 UK Biobank participants aged ≥40 years between 2006 and 2010. PRS for type 2 diabetes was calculated by summing weighted genetic variant effects. Incident all-cause and cause-specific dementias were identified using registry records up to December 2022. LE8 scores were classified as low vs. moderate-to-high levels. Cox regression and restricted cubic splines were applied. Results: Over an average follow-up of 13.27 years (SD = 2.27), 9425 participants developed dementia. A dose–response relationship was observed between PRS and vascular dementia, with risk rising sharply beyond the 95th percentile. Individuals with low LE8 constantly showed a higher risk of all-cause dementia than those with moderate-to-high LE8 across all values of PRS for type 2 diabetes. APOE ε4 accounted for more than 35% of the population-attributable risk of dementia, whereas the PRS for type 2 diabetes contributed only 1%. The population-attributable risk of all-cause dementia could be further reduced by 5.91% to 10.46% through maintaining moderate-to-high LE8 behavioral components, even after considering APOE ε4. Conclusions: A dose–response relationship exists between PRS for type 2 diabetes and dementia, particularly vascular dementia. Adherence to optimal LE8 metrics, particularly behavioral components, may contribute to dementia prevention across genetic strata. These findings highlight the importance of multidomain lifestyle interventions in dementia prevention. Full article

Lactate is increasingly recognized as a signaling molecule capable of modulating gene expression and vascular function. This descriptive pilot study investigated the effects of different lactate concentrations (0 mM, 10 mM, 20 mM, and 30 mM) and exposure times (1 h, 3 h, and 6 h) on the transcriptomic responses of human umbilical vein endothelial cells (HUVECs). Using next-generation RNA sequencing, an unbiased genome-wide analysis was performed, followed by focused examination of genes relevant to endothelial biology, calcium signaling, and glycocalyx integrity. Results showed that there was no statistically significant effect of lactate concentration on the expression of the examined genes. In contrast, prolonged incubation time was associated with differential expression of KLF2, KLF4, FOXO1, CD34, and VCAM1. These findings suggest that exposure time, rather than lactate concentration, may be associated with endothelial gene expression patterns under static conditions. This exploratory pilot study provides preliminary transcriptomic observations and highlights the need for further mechanistic investigations including functional and protein-level analyses. Full article