Search Results (87)

This study examined the effects of cognitive fatigue on repeated sprint ability (RSA), neuromuscular performance, and vigilance in physically active young adults (N = 28, 16 males, 12 females; mean age = 20.6 ± 1.4 years). Participants were randomly assigned to a mental fatigue (MF) or control (CON) group and completed baseline and post-condition assessments following a cognitively demanding or neutral task. Repeated sprint performance significantly declined in the MF group, as shown by increased RSA mean time (Δ = 0.432 s, p < 0.001) and total time (Δ = 4.331 s, p < 0.001), with no statistically significant change observed in the CON group. Countermovement jump height remained unaffected; however, repeated jump ability showed impaired contact time (Δ = 0.084 s, p = 0.007) in the MF group. Psychomotor vigilance significantly deteriorated under mental fatigue, as evidenced by slower reaction times (Δ = 119.71 ms, p < 0.001) and increased lapses (Δ = 2.86, p < 0.001). Subjective ratings confirmed elevated perceived exertion (Δ = 0.79, p = 0.002) and mental fatigue (Δ = 8.00, p < 0.001) in the MF group, without changes in motivation. These findings may demonstrate that cognitive fatigue impairs both physical and cognitive performance, even in trained individuals. Full article

Event-Sourced Systems (ESSs) that adopt Domain-Driven Design (DDD) are becoming more popular because of their intuitive business process modeling and improved auditability, scalability, and flexibility. However, ensuring the correctness of domain models—particularly event-sourced aggregates (ESAs)—remains challenging. To address this, we propose root contracting, a novel, constrained, and lightweight adaptation of Design by Contract (DbC), specifying the precondition, postcondition, and class invariant exclusively at aggregate roots. Root contracting simplifies correctness enforcement by leveraging DDD principles aligned with DbC and the standardized ESA code structure. We offer uContract, a Java open-source utility that realizes root contracting, enabling automated verification of ESAs with configurable runtime overhead. Through performance evaluation and methodological discussion, we demonstrate that root contracting effectively bridges formal correctness with practical domain modeling. Our approach provides developers with a tool to streamline development workflows, potentially reducing testing overhead and supporting integration with methodologies like Behavior-Driven Development (BDD). Full article

Objective: Mental fatigue (MF) worsens soccer performance. Further knowledge is needed to understand MF’s effects on soccer players and its underlying mechanisms. Our aim was to analyze the subjective, objective, and neural MF-related outcomes induced by different type of tasks. Methods: A randomized crossover experimental design with repeated measures was used. Thirteen amateur soccer players (M_age = 23 ± 5.43) completed three conditions: cognitive (30 min. Stroop.), physical (30 min. cycling), or combined (30 min. Stroop while cycling). Ratings of mental fatigue (measured via the Visual Analogue Scale), electroencephalographical signals (electroencephalography), and psychomotor performance (Brief-Psychomotor Vigilance Test) were measured pre- and post-condition. Soccer-related decision-making (TacticUP^® test) was assessed post-condition. Results: Linear Mixed Models analysis revealed increments in perceived mental fatigue in all conditions, especially cognitive (p = 0.004) and combined (p < 0.0001) conditions. Psychomotor performance worsened, especially for cognitive (p = 0.039) and combined (p = 0.009) conditions. The Individual Alpha Peak Frequency was lower after the cognitive task (p = 0.040) and compared with the physical task (p = 0.021). The Alpha midline power increased after the cognitive task in the central-frontal (p = 0.047) and central-posterior brain regions (p = 0.043). Conclusions: Cognitive and combined conditions were found to be more mentally demanding and fatiguing than single physical tasks. This was also reflected by an impaired reaction time. Based on the neural activity recorded, the performance impairments caused by mental fatigue were caused by reduced brain readiness (i.e., a lower Alpha Peak Frequency). However, non-significant changes were found in soccer-related decision-making. Coaches should consider the type of training tasks they recommend in light of their different effects on mental fatigue and performance. Full article

The investigation of the reward system is a fascinating domain with future applications for pain therapy and understanding addiction. We investigated interactions between tramadol use and the imidazoline system, through the modulatory effects of imidazoline receptor blockers, by behavior analysis and electroencephalography (EEG). Thirty-six male Wistar rats were placed within a conditioned place preference (CCP) setting using a three-compartment box apparatus. The transition of the six groups of subjects from one compartment to another was constantly monitored, related to preconditioning for one day, conditioning for eight days, and post-conditioning testing on day 10. During the conditioning phase, the groups received: a saline solution, efaroxan, idazoxan, tramadol, tramadol + efaroxan, and tramadol + idazoxan, respectively. The administration of efaroxan, idazoxan, or a saline solution in the non-preferred compartment did not alter the time spent by rats there. On the other hand, the administration of tramadol alone in the non-preferred compartment significantly increased the time spent by animals there (151.66 ± 11.69 s) post-conditioning as compared to preconditioning (34.5 ± 5.31 s) (p < 0.01), while the combination of efaroxan and tramadol significantly reduced its effect. After the combination with idazoxan, the effect of tramadol on increasing the time spent by the animal in the non-preferred compartment remained significantly higher than in the preconditioning phase. A significant increase in time spent in the non-preferred compartment demonstrates the existence of a CPP induction effect (by changing the preference). The effects of tramadol on the reward system can cause changes in the brain’s neuroplasticity, potentially leading to learned behaviors that promote drug seeking in previous non-preferred environments. Full article

Over the past four decades, cardioprotective research has revealed an extraordinary complexity of cellular and molecular mechanisms capable of mitigating ischemia/reperfusion injury (IRI). Among these, ischemic conditioning has emerged as one of the most influential discoveries: brief episodes of ischemia followed by reperfusion activate protective programs that reduce myocardial damage. These effects can be elicited locally (pre- or postconditioning) or remotely (remote conditioning), acting mainly through paracrine signaling and mitochondria-linked kinase pathways, with both early and delayed windows of protection. We have contributed to clarifying the roles of mitochondria, oxidative stress, prosurvival kinases, connexins, extracellular vesicles, and sterile inflammation, particularly via activation of the NLRP3 inflammasome. Despite robust preclinical evidence, clinical translation of these approaches has remained disappointing. The challenges largely stem from experimental models that poorly reflect real-world clinical settings—such as advanced age, comorbidities, and multidrug therapy—as well as the reliance on surrogate endpoints that do not reliably predict clinical outcomes. Nevertheless, interest in multi-target protective strategies remains strong. New lines of investigation are focusing on emerging mediators—such as gasotransmitters, extracellular vesicles, and endogenous peptides—as well as targeted modulation of inflammatory responses. Future perspectives point toward personalized cardioprotection tailored to patient metabolic and immune profiles, with special attention to high-risk populations in whom IRI continues to represent a major clinical challenge. Full article

Background/Objectives: Ischemic postconditioning (IP) is a well-established intervention that mitigates this damage by activating endogenous cardioprotective pathways. However, the presence of comorbidities such as dyslipidemia can disrupt these protective mechanisms and abolish the infarct-sparing effect typically induced by IP. In this context, identifying pharmacological strategies to restore cardioprotection is of clinical relevance. This study aimed to evaluate whether N-acetylcysteine (NAC), a glutathione precursor with antioxidant properties, can restore the infarct-limiting effect of IP compromised by HFD-induced oxidative stress. Methods: Male mice were fed a control diet (CD) or HFD for 12 weeks. NAC (10 mM) was administered in drinking water for 3 weeks before ex vivo myocardial ischemia/reperfusion (I/R) injury (30 min ischemia/60 min reperfusion). In IP groups, six cycles of brief I/R were applied at the onset of reperfusion. Infarct size, ventricular function, redox status (GSH/GSSG), lipid profile, and histology were evaluated. Results: NAC improved the lipid profile (HDL/non-HDL ratio) and enhanced the infarct-sparing effect of IP in CD-fed mice. In HFD-fed mice, NAC restored the efficacy of IP, significantly reducing infarct size (HFD-I/R-NAC: 39.7 ± 4.5% vs. HFD-IP-NAC: 26.4 ± 2.0%, p < 0.05) without changes in ventricular function. The ratio of oxidized/reduced glutathione (GSSG/GSH) is depicted. Under basal conditions, the hearts of mice fed an HFD exhibited a shift towards a more oxidized state compared to the control diet CD group. In the I/R protocol, a significant shift towards a more oxidized state was observed in both CD and HFD-fed animals. In the IP protocol, the GSSG/GSH ratio revealed a tendency to basal values in comparison to the I/R protocol. The analysis indicates that animals subjected to I/R and IP protocols in conjunction with NAC show a tendency to reach basal values, thus suggesting a potential for the reduction in ROS. Conclusions: NAC treatment mitigates oxidative stress and restores the cardioprotective effect of ischemic postconditioning in a model of early-stage atherosclerosis. These findings support NAC as a potential adjunct therapy to improve myocardial resistance to reperfusion injury under dyslipidemic conditions Full article

Coronary artery disease remains a leading cause of morbidity and mortality worldwide. Acute myocardial infarction results in ischemia-induced cellular dysfunction and death. While timely reperfusion limits myocardial damage, it paradoxically triggers ischemia–reperfusion injury (IRI), exacerbating tissue damage. IRI, first observed in the 1960s, is mediated by complex molecular pathways, including oxidative stress, calcium dysregulation, endothelial dysfunction, and inflammation. This review examines emerging therapeutic strategies targeting IRI, including ischemic preconditioning, postconditioning, pharmacological agents, and anti-inflammatory therapies. Preconditioning serves as an endogenous protection mechanism, while pharmacological postconditioning has become a more clinically feasible approach to target oxidative stress, inflammation, and apoptosis during reperfusion. Pharmacological agents, such as GSK-3β inhibitors, JNK inhibitors, and mesenchymal stem cell-derived exosomes, have shown promise in modulating molecular pathways, including Wnt/β-catenin and NF-κB, to reduce myocardial injury and enhance recovery. Combination therapies, integrating pharmacological agents with mechanical postconditioning, provide a synergistic approach to further protect tissue and mitigate damage. However, translating preclinical findings to clinical practice remains challenging due to discrepancies between animal models and human conditions, particularly with comorbidities such as diabetes and hypertension. Continued research is essential to refine these therapies, optimize clinical application, and address translational challenges to improve outcomes in IRI. Full article

Background: Flywheel resistance training has gained popularity due to its ability to induce eccentric overload and improve strength and power. This study examined the acute effects of low- (0.025 kg·m²) versus high-inertia (0.10 kg·m²) flywheel deadlifts, matched for force impulse, on the countermovement jump (CMJ) performance, reactive strength index (RSI) during drop jumps (DJs), and rating of perceived exertion (RPE). Methods: Sixteen trained participants (twelve men, and four women) performed three conditions in a randomized, counterbalanced order: low-inertia (LOW), high-inertia (HIGH), and control (CTRL). In the LOW and HIGH conditions, we used force plates to measure and equalize the force impulse in the two conditions (HIGH: 20182 ± 2275 N∙s vs. LOW: 20076 ± 2526 N∙s; p > 0.05), by calculating the number of deadlift repetitions required to achieve it (HIGH: 5 repetitions and LOW: 9.8 ± 0.4 repetitions). The RSI and CMJ performance were measured pre-exercise, immediately post-exercise, and at 3, 6, 9, and 12 min post-exercise. Results: Both the RSI and CMJ performance improved equally after LOW and HIGH flywheel deadlifts compared to baseline and CTRL (p < 0.01). Specifically, the RSI increased from baseline at 3 to 12 min in both conditions (LOW: 12.8 ± 14.9% to 15.4 ± 14.8%, HIGH: 12.1 ± 17.0% to 12.2 ± 11.7%, p < 0.01), while the CMJ increased from 3 to 9 min in LOW (4.3 ± 3.2% to 4.6 ± 4.7%, p < 0.01) and from 6 to 9 min in HIGH (3.8 ± 4.2% to 4.2 ± 4.9%, p < 0.05). No significant differences were observed between LOW and HIGH conditions (p > 0.05), suggesting similar effectiveness of both inertial loads for enhancing performance. The RPE increased similarly after both conditions from baseline to immediately post-conditioning (LOW: from 2.2 ± 1.2 to 5.8 ± 1.4, HIGH: from 1.5 ± 1.0 to 6.1 ± 1.5, p < 0.01) and decreased by the end of the session, although values remained higher than baseline (LOW: 4.1 ± 1.4, p < 0.01, HIGH: 4.5 ± 2.0, p < 0.01). Conclusions: These findings highlight the potential of flywheel deadlift exercise as an effective method to potentiate explosive performance of the lower limbs, regardless of inertia, provided that the total force impulse is equal. Full article

Background: Our research team analyzed the microRNA (miRNA)-197-3p involved in cardioprotection, and we demonstrated that the overexpression of miRNA-197-3p could be linked to a higher risk of cardiac damage. Recent research indicated that miRNA-197-3p inhibits the effector proteins of the anaesthetic preconditioning mechanism of halogenated drugs. In this scenario, we proposed to determine the role of miRNA-197-3p in cardiac injury and its effects on myocardial conditioning under halogenated exposure. Hypothesis: Patients having myocardial revascularization surgery have increased heart damage due to postoperative miRNA-197-3p upregulation. Methods: Human cardiac myocytes (HCMs) were used in an in vitro hypoxia/reperfusion (H/R) model. The miRNA-197-3p-MIMIC was transfected into the HCMs. Three H/R-induced HCM groups were performed: negative MIMIC-control transfected, MIMIC transfected, and non-transfected. Each H/R cell group was exposed to Propofol (P), Sevoflurane (S), or non-exposed. Healthy cell cultures were the control group. ELISA assays were used to assess the Akt1 and p53 cell secretion capacity, and the Next Generation Sequencing assay was used to measure the differential expression of miRNA targets. Results: The secretion capacity of H/R-induced HCMs transfected with the MIMIC was higher under sevoflurane exposure regarding Akt-1 cytokine (I/R + S: 0.80 ± 0.06 ng/mL; I/R + P: 0.45 ± 0.28 ng/mL; p > 0.05), and lower regarding p53 cytokine (I/R + S: 38.62 ± 6.93 ng/mL; I/R + P: 43.34 ± 15.20 ng/mL; p > 0.05) compared to propofol. In addition, a significant gene overexpression of five miRNAs, in the sevoflurane group, was linked to cardioprotection: miRNA-29-3p, 24-3p, 21-3p, 532, and miRNA-335-5p. Conclusions: miRNA-197-3p inhibits the cardioprotection induced by halogenated exposure and can be considered a biomarker of cardiac damage. Additional research is required to validate our findings in other clinical settings. Full article

Background: There is clinical concern about the combined use of alcohol and opiates. Several lines of evidence support an interaction between alcohol and the endogenous opioid system. Thus, we hypothesized that ethanol, by causing the release of opioid peptides, may sensitize the system to the action of exogenous opioids such as morphine. Objectives: In this study, using the place conditioning paradigm, a model of reward, we determined whether a morphine challenge would alter the pre-established preference induced by ethanol conditioning in mice, and whether this response was mediated by the mu opioid receptor (MOP). Given that ethanol exposure stimulates the release of opioid peptides, we also assessed the role of beta-endorphin (β-END) and enkephalins (ENKs) in this response. Methods: Mice lacking MOPs, β-END, and/or ENKs, and their respective wild-type controls were tested for preconditioning place preference on day 1. Mice were then conditioned with ethanol (2 g/kg) versus saline on days 2 to 4 and then tested under a drug-free state for postconditioning place preference on day 5. On day 8, mice received a single injection of morphine (5 mg/kg) and were tested for place preference. On the test days, mice were placed in the central chamber and allowed to explore the chambers. The amount of time that mice spent in the drug-paired chamber was recorded. Results: We found that a challenge dose of morphine given on day 8 enhanced the conditioned place preference (CPP) response in mice previously conditioned with ethanol. This response was abolished in MOP-null mice, confirming the role of MOPs in this response. Although this enhanced response was not altered in mice lacking either β-END or ENKs compared to their wild-type littermates/controls, it was completely blunted in mice lacking both β-END and enkephalins. Conclusions: Together, these results suggest that these opioid peptides jointly mediate the crosstalk between the rewarding actions of morphine and ethanol. Full article

Traumatic optic neuropathy (TON) has been regarded a vision-threatening condition caused by either ocular or blunt/penetrating head trauma, which is characterized by direct or indirect TON. Injury happens during sports, vehicle accidents and mainly in military war and combat exposure. Earlier, we have demonstrated that remote ischemic post-conditioning (RIC) therapy is protective in TON, and here we report that AMPKα1 activation is crucial. AMPKα1 is the catalytic subunit of the heterotrimeric enzyme AMPK, the master regulator of cellular energetics and metabolism. The α1 isoform predominates in immune cells including macrophages (Mφs). Myeloid-specific AMPKα1 KO mice were generated by crossing AMPKα1^Flox/Flox and LysM^cre to carry out the study. We induced TON in mice by using a controlled impact system. Mice (mixed sex) were randomized in six experimental groups for Sham (mock); Sham (RIC); AMPKα1^F/F (TON); AMPKα1^F/F (TON+RIC); AMPKα1^F/F LysM^Cre (TON); AMPKα1^F/F LysM^Cre (TON+RIC). RIC therapy was given every day (5–7 days following TON). Data were generated by using Western blotting (pAMPKα1, ICAM1, Brn3 and GAP43), immunofluorescence (pAMPKα1, cd11b, TMEM119 and ICAM1), flow cytometry (CD11b, F4/80, CD68, CD206, IL-10 and LY6G), ELISA (TNF-α and IL-10) and transmission electron microscopy (TEM, for demyelination and axonal degeneration), and retinal oxygenation was measured by a Unisense sensor system. First, we observed retinal morphology with funduscopic images and found TON has vascular inflammation. H&E staining data suggested that TON increased retinal inflammation and RIC attenuates retinal ganglion cell death. Immunofluorescence and Western blot data showed increased microglial activation and decreased retinal ganglion cell (RGCs) marker Brn3 and axonal regeneration marker GAP43 expression in the TON [AMPKα1^F/F] vs. Sham group, but TON+RIC [AMPKα1^F/F] attenuated the expression level of these markers. Interestingly, higher microglia activation was observed in the myeloid AMPKα1^F/F KO group following TON, and RIC therapy did not attenuate microglial expression. Flow cytometry, ELISA and retinal tissue oxygen data revealed that RIC therapy significantly reduced the pro-inflammatory signaling markers, increased anti-inflammatory macrophage polarization and improved oxygen level in the TON+RIC [AMPKα1^F/F] group; however, RIC therapy did not reduce inflammatory signaling activation in the myeloid AMPKα1 KO mice. The transmission electron microscopy (TEM) data of the optic nerve showed increased demyelination and axonal degeneration in the TON [AMPKα1^F/F] group, and RIC improved the myelination process in TON [AMPKα1^F/F], but RIC had no significant effect in the AMPKα1 KO mice. The myeloid AMPKα1c deletion attenuated RIC induced anti-inflammatory macrophage polarization, and that suggests a molecular link between RIC and immune activation. Overall, these data suggest that RIC therapy provided protection against inflammation and neurodegeneration via myeloid AMPKα1 activation, but the deletion of myeloid AMPKα1 is not protective in TON. Further investigation of RIC and AMPKα1 signaling is warranted in TON. Full article

Phosphorous is essential for many metabolic functions and the constitution of bones. Poultry have limited ability to use phosphorous from diets, which is mainly excreted and causes environmental concern. For this reason, diets are commonly supplemented with inorganic phosphorus and phytases. It has been suggested that chickens can adapt to an early nutrient restriction by increasing its efficiency of utilization, an adaptation that has been defined as nutritional conditioning. The aim of this study was to investigate a strategy of phosphorous nutritional conditioning by feeding low phosphorous diets during the first week of life as a strategy to improve the efficiency of phosphorous utilization later in life. To test this, 600 male broiler chickens were fed either a standard (control group) or a phosphorous-deficient diet (conditioned group) during the first week of life. Later in life, the effect of conditioning was tested using standard or P-deficient diets during the finishing phase (21–43 d). Conditioning did not affect overall performance, despite finding evidence for reduced relative phosphorous excretion between days 19 to 21, increased duodenal gene expression for the phosphorous transporter SLC34A2 at day 30 (−6% and +17%, respectively), and tendencies for improved phosphorous digestibility (+7%) and tibia mineralization (+6%) at the end of the trial. It is concluded that phosphorous nutritional conditioning early in life can increase subsequent dietary phosphorous utilization and bone mineralization in poultry, although it may not be able to counteract severe phosphorous deficiencies. Further research is required to assess the extent to which phosphorous supplementation in post-conditioning diets may be reduced with this strategy without compromising performance. Full article

This paper presents results from a case study focusing on analyzing impacts of Green Infrastructure (GI) on sensible and latent heat fluxes, urban microclimate and the subsequent water–energy nexus components of an urban infrastructure system. The case study, focusing on the campus of a public university in San José, CA, aimed to quantify the pre- and post-conditions for a hypothetical GI implementation, which is in support of San José State University’s (SJSU) robust sustainability initiatives, which are also aligned with Silicon Valley’s broader strategic goals. The results revealed that a reduction of 0.3 °C in the average daily peak maximum temperature on campus could be achieved by the GI implementation. Air-conditioning related energy use was projected to decrease by 1.28%, monthly water use by 7052 m³, and it would result in an estimated reduction of approximately 2800 kWh in the water–energy nexus. In addition to lowering the campus’s carbon footprint, GI therefore offers significant economic and environmental benefits in terms of reductions in the urban air temperature, energy usage and water demand. This study provides valuable information for policy makers and low impact development water infrastructure managers considering GI implementation. Full article

Background and Objective: Stroke poses a critical health issue without effective neuroprotection. We explore ischemic postconditioning’s (IPostC) potential to mitigate stroke-induced brain injury, focusing on its interaction with disulfidptosis, a novel cell death pathway marked by protein disulfide accumulation. We aim to clarify IPostC’s protective mechanisms against stroke through gene sequencing and experimental analysis in mice. Methods: Through our initial investigation, we identified 27 disulfidptosis-related genes (DRGs) and uncovered their interactions. Additionally, differential gene analysis revealed 11 potential candidate genes that are linked to disulfidptosis, stroke, and IPostC. Our comprehensive study employed various analytical approaches, including machine learning, functional enrichment analysis, immune analysis, drug sensitivity analysis, and qPCR experiments, to gain insights into the molecular mechanisms underlying these processes. Results: Our study identified and expanded the list of disulfidptosis-related genes (DRGs) critical to stroke, revealing key genes and their interactions. Through bioinformatics analyses, including PCA, UMAP, and differential gene expression, we were able to differentiate the effects of stroke from those of postconditioning, identifying Peroxiredoxin 1 (PRDX1) as a key gene of interest. GSEA highlighted PRDX1’s involvement in protective pathways against ischemic damage, while its correlations with various proteins suggest a broad impact on stroke pathology. Constructing a ceRNA network and analyzing drug sensitivities, we explored PRDX1’s regulatory mechanisms, proposing novel therapeutic avenues. Additionally, our immune infiltration analysis linked PRDX1 to key immune cells, underscoring its dual role in stroke progression and recovery. PRDX1 is identified as a key target in ischemic stroke based on colocalization analysis, which revealed that PRDX1 and ischemic stroke share the causal variant rs17522918. The causal relationship between PRDX1-related methylation sites (cg02631906 and cg08483560) and the risk of ischemic stroke further validates PRDX1 as a crucial target. Conclusions: These results suggest that the DRGs are interconnected with various cell death pathways and immune processes, potentially contributing to IPostC regulating cell death mechanisms in stroke. Full article

Endothelial dysfunction (ED) is closely associated with most cardiovascular diseases. Experimental models are needed to analyze the potential impact of ED on cardioprotection in constant pressure Langendorff systems (CPLS). One cardioprotective strategy against ischemia/reperfusion injury (I/RI) is conditioning with the lipid emulsion Intralipid (IL). Whether ED modulates the cardioprotective effect of IL remains unknown. The aim of the study was to transfer a protocol using a constant flow Langendorff system for the induction of ED into a CPLS, without the loss of smooth muscle cell functionality, and to analyze the cardioprotective effect of IL against I/RI under ED. In isolated hearts of male Wistar rats, ED was induced by 10 min perfusion of a Krebs–Henseleit buffer containing 60 mM KCl (K+), and the vasodilatory response to the vasodilators histamine (endothelial-dependent) and sodium–nitroprusside (SNP, endothelial-independent) was measured. A CPLS was employed to determine cardioprotection of pre- or postconditioning with 1% IL against I/RI. The constant flow perfusion of K+ reduced endothelial response to histamine but not to SNP, indicating reduced vasodilatory functionality of endothelial cells but not smooth muscle cells. Preconditioning with IL reduced infarct size and improved cardiac function while postconditioning with IL had no effect. The induction of ED neither influenced infarct size nor affected the cardioprotective effect by preconditioning with IL. This protocol allows for studies of cardioprotective strategies under ED in CLPS. The protection by preconditioning with IL seems to be mediated independently of a functional endothelium. Full article