Search Results (982)

Uplift modeling optimizes intervention-based campaigns by identifying customers whose behavior changes exclusively due to specific treatments, moving beyond standard baseline risk predictions. However, in real-world deployments, algorithms that maximize traditional causal ranking metrics (e.g., the Qini coefficient) often fail to be optimal in practice. The inherent variance of Conditional Average Treatment Effect (CATE) estimators exposes critical trade-offs between expected economic value, algorithmic stability, and policy interpretability. To address this gap, this study proposes a stability-aware, value-driven computational framework for selecting an uplift policy. The pipeline evaluates multiple causal and non-causal algorithmic families, including traditional baselines, multimodel approaches, and transformed-outcome variants, within a repeated-run validation protocol. Candidate policies are assessed primarily through incremental revenue and target-set stability, whereas a post hoc surrogate tree distillation step is used to translate the selected policy into interpretable rule-based customer segments. An empirical evaluation of the publicly available Telco Customer Churn dataset under two distinct regimes (a causally controlled semisynthetic scenario and an observational proxy scenario) reveals that the highest-yielding causal policy frequently suffers from severe targeting instability, inducing a clear risk–return trade-off. Furthermore, uplift models outperform traditional baselines in the causally controlled regime, whereas traditional baselines remain economically superior in the confounded proxy settings. Overall, this study establishes that jointly assessing economic utility, algorithmic stability, and transparent segmentation is essential for deploying robust and defensible causal machine learning in production environments. Full article

Once written off as nothing more than a waste product of glycolysis, lactic acid is now seen as a key signaling molecule that operates across a wide range of physiological and pathological processes, from immune regulation and tumor metabolism to neural function. But its role goes beyond energy metabolism and cell signaling. Recent studies have uncovered a new type of post-translational modification called histone lactylation, in which lactate itself provides the lactoyl group attached to lysine residues on histones. This modification directly ties a cell’s metabolic state to the epigenetic control of gene expression. For example, histone lactylation helps shift macrophages from a pro-inflammatory M1 phenotype to an anti-inflammatory M2 phenotype by fine-tuning gene transcription. In this review, we walk through the discovery and biochemical foundation of histone lactylation; discuss the likely writer and eraser enzymes that manage its dynamic changes; and highlight recent advances in understanding the role of this modification in inflammation, tumorigenesis, neurological disorders, and interactions with gut microbes. We also lay out key unanswered questions and consider why targeting protein lactylation might open up new therapeutic possibilities. Full article

Spi-1 Proto-Oncogene (SPI1) encodes Purine-rich box 1 Transcription Factor (PU.1), a transcription factor of the ETS family that regulates hematopoietic lineage commitment and immune cell differentiation. Alteration of PU.1 dose or ETS domain integrity may interfere with transcriptional programs, which adds to hematopoietic dysregulation and leukemogenesis. Even though changes in SPI1 expression have been associated with acute myeloid leukemia (AML), the structural and regulatory effects of missense mutations at the PU.1 ETS domain have not been entirely studied, and targeting the PU.1 ETS domain by ligands is an area of computational analysis that should be further pursued. To computationally describe deleterious missense variants of SPI1 in terms of structural stability, evolutionary conservation, post-translational modification (PTM) context and interaction networks, and to measure ADMET-mediated molecular docking of cinnamic acid with the PU.1 ETS domain (8EQG) as a potential modulator. Missense nsSNPs were obtained through Ensembl and narrowed down by consensus prediction of pathogenicity (PredictSNP, combining SIFT, PolyPhen, SNAP and PhD-SNP and other tools). InterPro/UniProt was used for domain mapping. SWISS-MODEL was used to produce wild-type and mutant PU.1 versions, which were analyzed on the structural alignment and Cα–Cα displacement parameters in UCSF Chimera (v1.19). The estimation of stability change was carried out with I-Mutant and MUpro. Prediction of PTM sites was done using MusiteDeep and exploration of functional partners was done using STRING. Human, mouse and zebrafish orthologue conservation was measured by means of MAFFT alignment. GEPIA2 was used to compare the expression of SPI1 in AML (TCGA-LAML) and normal tissues (GTEx). AutoDock Vina (grid center 6, −2, −9 A; 20 × 20 × 20 A; 16 exhaustiveness) was used to prepare cinnamic acid and dock it into the PU.1 ETS domain (8EQG), with SwissDock being used for consistency checks. SwissADME and ADMETlab 2.0 were used to predict drug-likeness, pharmacokinetics, and toxicity. Nine missense mutations were routinely considered as deleterious with the majority of them being located in or near the ETS DNA-binding domain. Structural comparisons showed local perturbations of the structure and I189F and H211P yielded the greatest conformational changes between prioritized variants whereas other forms had minimal movements. A predominantly destabilizing trend was supported by stability prediction whereby V241G had the strongest destabilization signal with further destabilizations being predicted in I189F and R259C. PTM mapping revealed several potential regulatory residues (phosphorylation, acetylation, ubiquitination, and methylation), which indicated that there could be crosstalk between the sequence variation and the transcriptional regulation. The SPI1 was placed in a central hematopoietic transcriptional module (containing RUNX1, CEBP members, GATA1 and IRF factors) by the STRING network. The cross-species alignment showed that there was high conservation of a number of the mutation sites, which would support functional constraint at the ETS region. The expression analysis revealed that the level of SPI1 mRNA in AML was significantly elevated compared to normal tissues. Docking also indicated a slight and reproducible interaction of cinnamic acid with the ETS domain (top affinity −4.27 kcal/mol), with a solitary leading polar anchor and supportive hydrophobic interactions, which is akin to interaction between fragments. The ADMET profiling revealed the likelihood of success in the oral drug-likeness and low CYP inhibition liability, as well as signifying the presence of a possible hepatotoxicity signal that needs further confirmation through experiments. Comprehensive computational studies suggest that certain pathogenic variants of SPI1 missense defects, especially in the ETS domain, can result in loss of PU.1 structural stability and regulatory environment, which are in line with the disturbed hematopoietic regulation and AML-related dysregulation. Cinnamic acid demonstrates moderate yet reproducible binding to the PU.1 ETS domain and has an overall favorable developability profile, which indicates that it is better considered as a starting scaffold, as opposed to an active inhibitor. The results give a logical basis of focused biochemical validation and structure-directed optimization of ETS domain modulators in hematologic disease settings. Full article

Cardiac fibroblast activation into α-smooth muscle actin (α-SMA)-expressing myofibroblasts is a central event in the progression of cardiac fibrosis. Therapeutic strategies capable of reversing or inhibiting this phenotypic transition are therefore of critical interest. Here, we explore associative changes in transcriptional and post-transcriptional regulators linked to fibroblast activation following atorvastatin exposure in primary human cardiac fibroblasts (HCFs). Atorvastatin treatment (10 µM) was associated with a reduction in α-SMA expression, consistent with decreased myofibroblast activation. This change co-occurred with reduced expression of the transcription factors GATA4 and MEF2C, which are implicated in cardiac cell identity and plasticity. Concurrently, atorvastatin treatment was associated with selective increase in specific fibrosis-related microRNAs, including miR-24, miR-26a, and miR-133a, whereas the expression of miR-21 and miR-23a remained unchanged. Together, these findings describe a coordinated pattern of transcriptional and post-transcriptional changes associated with atorvastatin exposure in HCFs, consistent with a shift away from the myofibroblast phenotype. These observations provide descriptive, hypothesis-generating insight into potential regulatory patterns associated with atorvastatin treatment, although further functional studies are required to establish causal relationships and translational relevance. Full article

Public administration research provides structured explanations of collaborative governance. PPP scholarship, however, has largely emphasized macro governance frameworks, leaving micro-level collaborative drivers between internal partners underexplored. Additionally, internal transparency has seldom received attention as a governance outcome of collaboration. Building upon collaborative governance theories, this study conceptualizes collaboration in PPPs through four focal collaborative elements (FCEs): organizational capacity asymmetries, commitment to process, effective communication, and trust building. A survey instrument was used to collect experts’ opinions regarding the impact of PPP-specific characteristics, as practical mechanisms, on collaboration. The results show strong endorsement of mechanisms related to post-procurement capacity asymmetries, role/authority shifts, contractual complexity, and lifecycle discontinuities (staff changes and phase transitions). Such PPP characteristics undermine communication and information continuity. Trust building appeared to have an ambivalent role shaped by long-term incentives alongside goal drift and contractual rigidity. This study identifies the most salient mechanisms framing collaborative elements in PPP and translates them into governance implications for sustained collaboration and strengthened internal transparency across PPPs’ lifecycle. Limitations and future avenues for research based upon these findings are presented. Full article

Background/Objectives: Bile acids, synthesized from cholesterol in the liver, are amphipathic molecules that play an integral role in lipid digestion and absorption, while also serving as systemic endocrine hormones. They continuously undergo enterohepatic circulation, where they interact with various transporter proteins. Dysregulated bile acid transport is associated with the pathogenesis of liver disease. This review summarizes the key findings relating to bile acid transport expression and activity in the pathogenesis of liver disease. Methods: A review of the literature was performed using PubMed and relevant terms including, but not limited to, “bile acid transporters”, “liver disease”, and “bile acid uptake and efflux”. Studies published in peer-reviewed journals relevant to this review were considered and reviewed. Results: Within the gut and liver, several key bile acid and xenobiotic transporters within the enterohepatic circulation are dysregulated. The directionality and extent of changes are cell- and disease-specific. Many of the regulatory processes are driven by changes in bile acid signaling, although further work is needed to expand on post-translational modification of bile acid transporters in liver disease. Conclusions: Bile acid transporters are dynamically regulated in liver diseases with distinct etiologies. Therefore, restoring BA transporter function represents an actionable therapeutic approach to liver disease. Full article

Background: Post-approval manufacturing changes for biologics require rigorous comparability assessments to ensure uninterrupted quality and clinical performance. CMAB007 (Aomaishu^®), a China-approved (2023) omalizumab biosimilar, underwent process enhancements—including media optimization and anion-exchange chromatography substitution—yielding a 5-fold increase in production without altering the host cell line. Methods: A novel three-arm tiered strategy was adopted to compare post-change CMAB007, pre-change CMAB007, and reference (Xolair^®) products. Critical quality attributes (CQAs) were classified into tiers based on risk impact, with tier-specific acceptance criteria. Comprehensive analytics assessed structure, post-translational modifications, purity/impurities, activity, and Fc-mediated functions. Forced degradation (lyophilized/reconstituted states) and accelerated stability studies were evaluated. Based on the high degree of CMC similarity and to prevent “biological drift”, the pharmacokinetic (PK) and safety comparability of the post-change CMAB007 versus the reference product (Xolair^®) was confirmed in a randomized, double-blind, two-arm study in healthy males (N = 114; single 150 mg subcutaneous administration). The pre-change product was not included in this clinical PK study. Results: Post-change CMAB007 exhibited analytical similarity within tiered acceptance criteria for all CQAs. Stability studies confirmed enhanced robustness under stress conditions. PK equivalence was demonstrated for AUC_0–inf (GMR: 99.82%; 90% CI: 91.46~108.94%), AUC_0–t (99.54%; 91.40~108.41%), and C_max (101.88%; 95.21~109.01%). Immunogenicity (ADA incidence: 10.5% vs. 12.5%, p = 0.742) and safety profiles were comparable. Conclusions: This study pioneers a tiered three-arm comparability strategy for post-approval changes, integrating advanced analytics, risk-based quality assessment, and clinical validation. The approach mitigates “biological drift” risks, ensuring biosimilar quality, efficacy, and safety while enabling sustainable production scalability. Full article

Background/Objectives: Both adiposity and nutritional–inflammatory status influence glucose metabolism; however, their longitudinal associations with glycemic changes in non-diabetic populations remain unclear. We examined the independent, interactive, and joint associations of body mass index (BMI) and prognostic nutritional index (PNI) with the 3-year change in HbA1c (ΔHbA1c). PNI, a composite marker of serum albumin and peripheral lymphocyte count, reflects both protein nutritional status and systemic immune competence. We hypothesized that BMI and PNI would each independently predict ΔHbA1c and that their joint profiling would identify higher-risk subgroups. Methods: A total of 9414 non-diabetic adults from the Shanghai Suburban Adult Cohort were included. Participants with diabetes at baseline (defined as fasting plasma glucose ≥ 7.0 mmol/L, 2-h post-load glucose ≥ 11.1 mmol/L, HbA1c ≥ 6.5%, or self-reported physician diagnosis of diabetes or use of glucose-lowering medications) were excluded. BMI was measured, and PNI was calculated as serum albumin + 5 × lymphocyte count. ΔHbA1c was assessed over a 3-year period. Multivariable linear regression, interaction testing, and joint stratification were performed. Covariate selection was guided by prior biological plausibility, and model adequacy was evaluated using the Akaike Information Criterion (AIC). Results: Both BMI (β = 0.013% per kg/m², 95% CI: 0.011–0.016, p < 0.001) and PNI (β = 0.002% per unit, 95% CI: 0.000–0.004, p = 0.019) were independently and positively associated with ΔHbA1c. No significant interaction was observed (p = 0.431). High BMI (≥24 kg/m²) was associated with glycemic worsening irrespective of PNI level (β ≈ 0.075%, p < 0.001). Among normal-weight individuals, higher PNI was associated with a modest increase in ΔHbA1c (β = 0.031%, p = 0.007). Conclusions: Although the absolute effect sizes were modest at the individual level, BMI was consistently and independently associated with glycemic deterioration therefore, even small per-unit increases may translate into meaningful risk at the population level given the high prevalence of overweight and obesity. PNI showed a small positive association, suggesting that in relatively healthy populations a higher PNI may partly capture subtle pro-glycemic factors—such as low-grade inflammation or higher protein intake—rather than representing unambiguous nutritional benefit. The absence of interaction suggests that BMI and PNI act through largely independent pathways. These findings extend prior evidence by demonstrating that PNI provides modest additional glycemic information beyond BMI in non-diabetic community-dwelling adults, particularly among those of normal weight. Full article

A novel graphene-based nanomaterial, trade registered Hastalex^®, has been synthesised and investigated for its application as a 3D scaffold in surgical implantation. Hastalex is developed through the covalent bonding of amine-group-functionalised graphene oxide to the base chemical, poly(carbonate-urea)urethane. The material is under development for medical application including tendon, heart valve, and pelvic implant for prolapse surgery. For successful clinical translation, long-term rheological and chemical stability must be demonstrated and until now no systematic multi-year evaluation has been reported for graphene-poly(carbonate-urea)urethane nanocomposites. The material was synthesised in accordance with the patented formulation and evaluated at 0, 6, 12, and 24 months post-synthesis. Physicochemical properties were assessed using attenuated total reflectance Fourier-transform infrared spectroscopy, scanning electron microscope, contact angle measurements, thermogravimetric analysis, and mechanical analysis with tensile tests. Flow behaviour of Hastalex was evaluated using a rheometer to determine viscosity, shear stress response and impact of temperature changes and ageing on these factors. Hastalex exhibited non-Newtonian, shear-thinning behaviour consistent across all timepoints. Viscosity was found to increase progressively with ageing, attributed not to chemical degradation, but likely due to gradual solvent evaporation and densification of the polymer matrix during storage under ambient conditions. Rheological measurements across increasing temperature regimes revealed a heat-sensitive decrease in viscosity, followed by a reversal of changes beyond ~80 °C—likely due to enhanced solvent evaporation and chain reorganisation. This comprehensive material characterisation supports Hastalex as a promising candidate for bioengineering applications. Full article

Background: Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition marked by heterogeneous behavioral symptoms and systemic comorbidities, including immune and gastrointestinal dysfunctions. Emerging studies suggest that glycosylation—a fundamental post-translational modification regulating cellular communication and immune responses—may play a role in ASD pathophysiology, yet its contribution remains underexplored. Methods: In this study, we developed an integrative transcriptomic and network analysis framework to investigate glycosylation-related gene expression changes and their functional associations in ASD. Using publicly available datasets from bulk and single-cell RNA sequencing of brain and blood tissues, we focused on four prior-knowledge gene subsets: glycogenes, extracellular matrix glycoproteins, immune response genes, and autism risk genes. Results: Differential expression and pathway enrichment analyses revealed consistent dysregulation of glycosylation pathways, including mucin-type O-glycan biosynthesis, glycosaminoglycan metabolism, GPI-anchor formation, and sialylation, across ASD tissues. These transcriptional changes were functionally linked to altered immune signaling (e.g., IL-17, Toll-like receptor, and complement pathways) and synaptic development pathways, forming a distinct glyco-immune axis. Network analysis identified key glycogenes such as GALNT10, NEU1, LMAN2L, and CHST1 as central molecular nodes, interacting with immune and neuronal regulators. Linkage disequilibrium analysis further revealed ASD-associated SNPs influencing the expression of these glycogenes in both blood and brain tissues. Conclusions: Together, these findings support a model in which disrupted glycosylation contributes to ASD pathophysiology by mediating immune dysregulation and altered neuronal connectivity. This study offers a systems-level framework to understand the molecular complexity of ASD and highlights glycogenes as potential biomarkers and targets for future therapeutic exploration. Full article

Ischemic stroke (IS) remains a major cause of global disability and mortality. While exogenous H₂S has demonstrated neuroprotective potential, the role of endogenous H₂S generated by cystathionine β-synthase (CBS) in cerebral ischemia–reperfusion injury (CIRI) remains incompletely elucidated. L-Cysteine (L-Cys), as a substrate for CBS, serves as a key precursor for endogenous H₂S. Using the established pre-clinical model of CIRI—middle cerebral artery occlusion/reperfusion (MCAO/R) in rats—we investigated the neuroprotective effects of brain-derived CBS-generated H₂S through neurological function scoring, 2,3,5-triphenylchlorotetrazole (TTC) staining, enzyme-linked immunosorbent assay (ELISA), and histopathological examination. Immunofluorescence, Western blot, and laser speckle contrast imaging were utilized to analyze the protein expression of ZO-1, claudin-5, CBS, vascular endothelial growth factor receptor-2 (VEGFR₂) and CD31, as well as cerebral blood flux changes. L-Cys treatment ameliorated neurological deficits, reduced cerebral infarct volume, decreased serum lactate dehydrogenase (LDH) and neuron-specific enolase (NSE) levels, attenuated histopathological damage, alleviated cerebral edema, and restored blood–brain barrier integrity via upregulation of tight junction proteins ZO-1 and claudin-5. Additionally, L-Cys improved MCAO/R-induced cognitive impairment and behavioral deficits. Furthermore, L-Cys upregulated CBS and VEGFR₂ expression, enhanced endogenous H₂S production, promoted post-ischemic cerebral angiogenesis, and improved cerebral blood flux recovery. CBS-derived H₂S promoted post-ischemic angiogenesis mediated by VEGFR₂, enhances cerebral reperfusion flux, and consequently ameliorated MCAO/R-induced CIRI in rats, providing experimental evidence for clinical translation. Full article

Defining the near-surface signal reflecting the deep sub-surface leakage is a critical challenge in the risk assessment of geologic carbon storage (GCS) projects, often exacerbated by decoupled deep-to-shallow modeling. This study quantifies the mass distribution and phase evolution of leaked CO₂ through deep reservoir-caprocks, intermediate aquifer, and near-surface soil, thereby showing the sub-surface retention characteristics and the detectability of near-surface signals. A geological model from the deep reservoir to the soil layer was constructed to simulate CO₂ leakage through the caprock and migration into overlying strata in 1000 years. Using the simulator of GPSFLOW, this study evaluates the evolution of fluid phases and the mass distribution during the injection for 100 years and the post-injection periods. The results indicate that (1) at the moment the injection ceases, 87.43–99.06% of the CO₂ remaining within the system is retained within the reservoirs, with less than 8.42% reaching the intermediate aquifer. Remarkably, although the CO₂ ultimately reaching the near-surface soil is less than 0.00073% of the total mass retained within the system, this mass accumulation translates to a concentration anomaly with a signal-to-noise ratio of 368 relative to the background baseline. (2) Sensitivity analysis reveals that the injection rate affects the timing of fluid transport—a tenfold increase in injection rate (from 3.17 to 31.7 kg/s) accelerates the upward movement of CO₂, advancing its arrival at the near-surface by 15 years without changing the overall mass partitioning. The permeability anisotropy ratio affects CO₂ migration and phase distribution—decreasing the vertical to horizontal permeability ratio (1, 0.5, 0.25, 0.125) reduces connectivity, which delays the upward transfer and increases the amount of the aqueous CO₂. However, specifically in the soil layer, the aqueous CO₂ accumulation reveals a non-monotonic trend that peaks at an intermediate ratio of 0.25. (3) CO₂ shows a cascading distribution across formations where reservoirs provide the primary storage, and the intermediate aquifer reduces the mass available for near-surface accumulation. This attenuation effect significantly reduces the CO₂ mass that reaches the soil layer, thereby controlling the strength and duration of near-surface environmental signals. This work offers a theoretical reference for formulating near-surface monitoring strategies for CO₂ leakage in GCS. Full article

Men who have used violence against intimate partners remain an under-researched population, despite their potential to advance understanding of motivations and relational dynamics underlying such behavior. This study employed semi-structured interviews and interpretative phenomenological analysis to examine the lived experiences of five adult men with histories of partner violence. A superordinate theme, Chaotic Interpersonal and Systemic Relationships, encompassed five experiential themes describing volatile partnerships shaped by mutual vulnerabilities. Participants commonly reported trauma histories and/or antisocial traits influencing partner selection, with abuse experienced as bidirectional. Disillusionment emerged when participants perceived that the mutual nature of violence was unacknowledged, limiting their engagement in meaningful change. Although behavior change programs were often understood at a conceptual level, participants struggled to translate insight into sustained behavioral transformation. Consistent with post-traumatic growth theory, participants described developing greater personal responsibility and more constructive views of relationships over time. Greater systemic recognition of bidirectional violence, identified in the literature as a prevalent form of intimate partner violence, may strengthen the therapeutic alliance and support more nuanced etiological inquiry. Shifting systemic responses from deficit-based, gendered models toward strength-based approaches may better harness men’s capacity for more permanent positive psychological and behavioral change. Full article

Infectious complications remain a principal determinant of late morbidity and mortality following major thermal injury, reflecting a convergence of barrier disruption, microbial adaptation, and host immune dysfunction. The post-burn environment creates a uniquely permissive niche for pathogen persistence, characterized by altered tissue perfusion, biofilm formation, and dynamic shifts in microbial ecology toward multidrug-resistant organisms. Concurrently, profound and evolving changes in host immunity and metabolism reshape both susceptibility to infection and response to therapy. This review integrates current evidence across pathophysiology, microbiology, diagnostics, and treatment, with a focus on challenges that limit effective infection control in burn patients. Particular attention is given to diagnostic uncertainty arising from overlap between sterile inflammation and true infection, the clinical implications of biofilm-associated tolerance, and the impact of burn-specific pharmacokinetic variability on antimicrobial efficacy. We further examine emerging diagnostic and therapeutic innovations, including host-response profiling, rapid molecular detection platforms, and next-generation anti-infective strategies targeting microbial virulence, biofilm structure, and host immune pathways. Despite substantial scientific advances, translation into clinical practice remains constrained by limited burn-specific trials, heterogeneous definitions, and systemic barriers to antimicrobial development. Collectively, these challenges underscore the need for integrated, precision-based approaches that combine early source control, individualized antimicrobial optimization, and advanced diagnostic frameworks. Future progress will depend on coordinated efforts to standardize definitions, generate high-quality multicenter data, and align innovation with clinical applicability across diverse healthcare settings. Full article

Background: Hypothermic machine perfusion (HMP) has been associated with reduced delayed graft function compared with static cold storage (SCS). However, the molecular mechanisms underlying these differences during cold preservation remain incompletely understood. This study compared cold-storage-related biochemical and histological changes in kidneys preserved by HMP versus SCS using a Lewis rat model prior to transplantation. Methods: Following isolation, rat kidneys were flushed with cold saline (4 °C). Left kidneys were preserved by HMP at constant flow using Belzer’s machine perfusion solution (MPS) at 4 °C, while right kidneys were stored using SCS in University of Wisconsin solution at 4 °C. After four hours of preservation, kidneys were processed for biochemical and histological analysis. Fresh biopsies were evaluated for mitochondrial complex respiration. Western blotting was performed to assess expression of NDUFS3, a complex I subunit. Histological staining for nitrotyrosine and kidney injury markers was compared across groups. Results: Mitochondrial complex respiration did not differ significantly between the SCS and HMP groups. Western blot analysis demonstrated significantly increased NDUFS3 expression in HMP-preserved kidneys compared with SCS and control kidneys. Histological evaluation revealed elevated tubular staining of nitrotyrosine and kidney injury markers in SCS kidneys relative to controls, whereas HMP preservation markedly attenuated these increases. Conclusions: HMP mitigates cold-storage-induced oxidative stress and reduces expression of kidney injury markers after four hours of preservation. These molecular findings suggest a protective effect of HMP during cold preservation. Future studies with longer preservation times and transplantation models are needed to determine whether these improvements translate into enhanced post-transplant kidney function. Full article