Search Results (10,890)

The overexpression of cyclin-dependent kinase inhibitor p16 (INK4a) is widely recognized as a surrogate marker for high-risk human papillomavirus (HPV) in anogenital malignancies, but its significance in invasive breast carcinoma is complex and remains frequently debated. While historically investigated as a viral proxy, emerging evidence suggests that elevated p16 levels in breast tissue may instead reflect intrinsic cell-cycle dysregulation and retinoblastoma (Rb) pathway disruption, though direct molecular confirmation is lacking in this area of research. This study aims to evaluate the role of p16 as an indicator of tumor aggressiveness for high-risk phenotypes. We conducted a retrospective study of 100 female patients with invasive breast carcinoma. Employing a purposive sampling strategy rather than a consecutive series, we analyzed a targeted cohort consisting predominantly of triple-negative breast cancer (TNBC) and high-grade tumors to evaluate biomarker patterns specifically in advanced disease contexts. Immunohistochemical assessment was performed using a standardized cumulative nuclear and cytoplasmic scoring system, with expression thresholds defined by receiver operating characteristic (ROC) curve analysis optimized for histological grade. p16 overexpression was a predominant characteristic of these aggressive tumors and was identified in 64% of cases. Statistical evaluation revealed a robust and significant correlation between p16 overexpression and the triple-negative molecular subtype, as well as a marked inverse relationship with estrogen receptor (ER) status. Although p16 levels were frequently associated with specific aggressive phenotypes, no statistically significant difference in overall survival was observed between expression groups, a finding attributable to the uniformly high-risk nature of the selected cohort. This study suggests an association between p16 expression levels and aggressive tumor features, although the study design limits causal inferences. A non-significant trend towards p16 overexpression was observed in ductal carcinomas compared to lobular subtypes, while high p16 expression was noted exclusively in G3 tumors within this selected cohort, a finding influenced by the purposive sampling strategy and the ROC-based cutoff definition. Tumor necrosis was more prevalent in p16-overexpressing tumors. Furthermore, p16 levels showed a strong inverse relationship with estrogen receptor (ER) status, as they were significantly elevated in ER-negative and triple-negative tumors compared to luminal phenotypes. Full article

Endometriosis is a chronic, estrogen-dependent inflammatory disease including aberrant local steroidogenesis, inflammation, angiogenesis, oxidative stress, and prostaglandin-mediated pain. Given the elevated adrenergic receptor expression in endometriotic lesions and the potential of terazosin to downregulate Steroidogenic Factor-1 (SF-1), this study aimed to evaluate terazosin as a non-hormonal therapy in a surgically induced rat endometriosis model. Forty female Wistar rats were randomized to sham, untreated endometriosis, leuprolide acetate or terazosin; two postoperative deaths yielded final group sizes of 10/9/10/9. Blinded histopathology verified successful lesion establishment. ELISA quantified SF-1, IL-6, IL-8, TNF-α, NF-κB, VEGF, HIF-1α, and PGE2 in lesion tissue, serum, and peritoneal lavage; oxidative status was assessed by TAS, TOS, and OSI. Compared with untreated endometriosis, terazosin significantly reduced SF-1, PGE2, IL-6, IL-8, TNF-α, VEGF and HIF-1α across compartments (all p < 0.001), comparable to leuprolide (p = 1.000). Terazosin also normalized oxidative stress by decreasing TOS/OSI and restoring TAS in tissue, serum, and peritoneal fluid (p < 0.001). NF-κB decreased in tissue and serum (p < 0.001) but not in peritoneal fluid (p = 0.206). Overall, terazosin produced leuprolide-like molecular benefits without hormonal suppression, supporting repurposing as a candidate non-hormonal therapy, while highlighting the need for longer-duration studies and randomized clinical trials given model and pain-assessment limitations. Full article

Angelman syndrome (AS) is a neurodevelopmental disorder caused by the loss of maternal UBE3A expression, leading to disrupted proteostasis and synaptic dysfunction. Adenosine is a ubiquitous neuromodulator whose G protein-coupled receptors (ARs) regulate neuronal differentiation and neurite outgrowth during development. Here, we investigated AR signaling and their influence on survival–autophagy balance and neuronal morphology in an AS cellular model. Using SH-SY5Y cells with silenced UBE3A, we found that UBE3A loss markedly decreased A1AR, A2BAR, and A3AR protein levels while significantly increasing A2AR expression. Ligand affinity was preserved across genotypes, but A1AR and A2AAR desensitization kinetics were significantly slower in UBE3A-deficient cells. These effects were associated with reduced recruitment of G protein-coupled receptor kinase 2 (GRK2) to the plasma membrane and decreased GRK2–AR association in UBE3A-deficient cells, suggesting a possible contribution of altered GRK2 dynamics to prolonged AR signaling. Functionally, A1AR and A2AR agonists preferentially promoted survival of UBE3A-deficient cells and modulated the MDM2–p53 axis and autophagy markers; A1R stimulation also increased neurite density in UBE3A-deficient cells. Together, these results identify AR-level alterations and defective desensitization machinery in AS neuronal cells and link receptor changes to downstream proteostasis and morphological phenotypes relevant to AS pathophysiology. Full article

Background: Despite significant advances in heart failure (HF) management, mortality and readmission rates remain persistently high. Low adherence has been recognised as a contributing factor, although supporting data remain limited. Objective: This study aimed to evaluate the impact of medication adherence on outcome following a HF hospitalisation. Methods: Patients who were discharged after HF hospitalisation were included in the study from a national multicentre HF cohort, and their records were matched with the National Healthcare System database, which includes all health-related claims and clinical events. Adherence to beta blockers, renin-angiotensin system inhibitors, and mineralocorticoid receptor antagonists were measured using the proportion of days covered (PDC). Low adherence was defined by PDC < 80% for at least one of the three HF drug classes. We then analysed the relationship between the PDC and outcome during a two-year follow-up period. Results: A total of 448 patients (median age: 73 years; 67% male; mean ejection fraction: 40%) were included. Of these patients, 152 (34%) were classified as having low adherence. The two-year mortality rate was comparable between the two groups (16.9% vs. 19.1% in adherent and low-adherent groups, respectively, p = 0.6). However, the rates of all-cause and HF rehospitalisations at two years were lower in the adherent group than in the group with low adherence (85.9% vs. 92.8%, p ≤ 0.01; 48.5% vs. 58.2%, p = 0.04, respectively). Conclusions: In patients discharged after acute HF, low adherence to HF drugs is frequent and worsens outcome, particularly the risk of rehospitalisation. Full article

Background and Objectives: Kawasaki disease (KD) is an acute systemic vasculitis in children, and approximately 10–20% of patients develop resistance to intravenous immunoglobulin (IVIG), which is associated with an increased risk of coronary artery complications. Natural killer (NK) cells play an important role in innate immune regulation, but the temporal dynamics of NK-cell regulatory receptors during KD and their relationship with IVIG response remain unclear. Materials and Methods: In this prospective observational study, we performed longitudinal immunophenotyping in children with KD treated at a tertiary referral center. Peripheral blood samples were obtained before IVIG administration (D0) and at three follow-up timepoints after treatment (D2, D14, and D56). NK-cell subsets and receptor expression—including the activating receptor NKG2D and inhibitory receptor NKG2A—were analyzed using multiparameter flow cytometry. Associations with IVIG response were evaluated using Firth penalized logistic regression for baseline predictors and linear mixed-effects models to assess longitudinal immune trajectories. Results: A total of 69 patients with KD were included, of whom 17 (24.6%) were classified as IVIG resistant. Baseline NK-cell subsets and receptor expression did not differ significantly between IVIG-sensitive and IVIG-resistant patients, although the NKG2D/NKG2A ratio tended to be lower in resistant patients (median 2.51 vs. 3.34, p = 0.054). Longitudinal mixed-effects analysis demonstrated significant temporal changes in NK-cell regulatory signaling following IVIG therapy. Both NKG2A (P(time) = 0.019) and NKG2D (P(time) < 0.001) expression showed significant time effects across the disease course. Importantly, the NKG2D/NKG2A ratio demonstrated a significant time-by-group interaction (P(interaction) = 0.030), indicating divergent trajectories of activating and inhibitory NK-cell signaling according to IVIG response. At the convalescent phase (D56), IVIG-resistant patients showed significantly higher NKG2A expression (p = 0.038) and a lower NKG2D/NKG2A ratio (p = 0.023) than IVIG-sensitive patients. Conclusions: While baseline NK-cell immunophenotypes were not associated with IVIG response, longitudinal analysis revealed that IVIG-resistant patients exhibited a distinct immune trajectory, characterized by increased NKG2A expression and a lower NKG2D/NKG2A ratio during the convalescent phase. These findings suggest that differences in IVIG responsiveness may be related to alterations in immune regulatory processes during the resolution phase of inflammation. However, the clinical implications of these findings remain to be established and require validation in larger, multicenter studies with longitudinal outcome data. Full article

Background: Edwardsiella piscicida is a significant intracellular pathogen of channel catfish (Ictalurus punctatus) and a major threat to U.S. aquaculture. A recently developed recombinant attenuated vaccine strain (χ16016) uses arabinose-regulated murA expression to trigger delayed cell wall lysis in vivo, ensuring biological containment while conferring strong protection against virulent challenge. Although its efficacy has been demonstrated, the host immune programs underlying protection remain incompletely defined. Methods: We used RNA sequencing to characterize tissue-specific transcriptomic responses in the intestines and kidneys of channel catfish at 7 days post-vaccination. Fish were vaccinated with χ16016 by either bath immersion or intracoelomic (IC) injection, and differentially expressed genes and enriched immune pathways were analyzed to determine how the vaccine delivery route shapes systemic and mucosal immune responses. Results: Across comparisons, 19,101 differentially expressed genes revealed pronounced route- and tissue-dependent immune remodeling. As aquaculture vaccination strategies increasingly prioritize scalability and practical deployment, understanding how the delivery route shapes immune outcomes is critical. Here, IC vaccination induced broader systemic transcriptional changes, particularly in the intestine, whereas bath immunization elicited a more focused yet coordinated mucosal response. Overall, intestinal tissue exhibited greater transcriptional responsiveness than kidney tissue, underscoring its central role in early vaccine-induced immunity. Functional enrichment analyses identified the activation of innate recognition pathways, MAPK and calcium signaling cascades, complement components, antigen processing machinery, and cell adhesion networks. Notably, bath immunization enriched the intestinal immune network for IgA production pathway, which represents an orthology-based mapping of conserved mucosal immune components, alongside the upregulation of IL-6, CXCL12–CXCR4, integrins (α4β7), MHC class II, complement C3, and polymeric immunoglobulin receptor (pIgR). Given that catfish rely primarily on IgM in mucosal immunity, these findings indicate the induction of IgM-mediated mucosal defense rather than classical mammalian IgA responses. Concurrent complement and scavenger receptor signatures suggest a transition toward efficient opsonophagocytic clearance with controlled inflammation at this subacute stage. Conclusions: This study provides the first systems-level view of host transcriptomic responses to a regulated-lysis E. piscicida vaccine in channel catfish. The findings demonstrate that immersion vaccination, although transcriptionally less expansive than injection, effectively activates coordinated mucosal innate and adaptive immune programs, supporting its practical use as a scalable vaccination strategy for aquaculture. Full article

Background/Objectives: The androgen receptor (AR)-driven transcriptional program plays a pivotal role in the development and progression of prostate cancer. The binding of androgen dihydrotestosterone (DHT) to AR initiates transcriptional activation, thereby altering the transcriptional landscape. DHT-induced long non-coding RNAs (lncRNAs) have been recognized as crucial players in prostate cancer pathogenesis. This study aims to identify and explore the important role of such lncRNAs in prostate cancer. Methods: This study first analyzed transcriptome data from an androgen-dependent cell line, LNCaP, treated with different DHT concentrations and found a batch of lncRNAs exhibiting DHT concentration dependence. TCGA data suggested a correlation between the DHT-induced lncRNA and prostate cancer. Finally, a series of in vivo and in vitro experiments confirmed the effect and mechanism of lncRNA in prostate cancer. Results: AC092718.4 was highly expressed in AR-positive prostate cancer cell lines and tissues, and its expression in patients with Gleason scores 6–9 was significantly higher than in a normal control group. Notably, the expression level of AC092718.4 was upregulated in a concentration-dependent manner with DHT. In vitro experiments revealed that overexpression of AC092718.4 promoted cell proliferation and inhibited cell apoptosis. Conversely, knockdown of AC092718.4 suppressed tumorigenesis in vivo. Furthermore, our investigation into the pathogenetic mechanism demonstrated that AC092718.4 could act as an miRNA sponge for miR-138-5p, attenuating its inhibitory effect on downstream oncogenes, such as FERMT2, RHOC, and HIF1A. These AC092718.4/miR-138-5p/mRNA axes, in turn, facilitated the progression of prostate cancer. Conclusions: For the first time, we demonstrate that AC092718.4 may function as an oncogenic factor in prostate cancer. The AC0927.8.4/miR-138-5p/mRNA axes potentially offer promising diagnostic and therapeutic targets for prostate cancer. Full article

Ooencyrtus kuvanae is an egg parasitoid species that attacks the egg masses of Dendrolimus spp and Lymantria spp. in China, which gives it a temporal niche advantage against pest infestations by Dendrolimus spp. and Lymantria spp. Moreover, it has a short life cycle, high offspring outcome, and female-biased population, showing distinctive ovarian development and oviposition behaviors and thus providing an ideal model for reproductivity and regulatory mechanisms. Previous studies have found that the Vitellogenin (Vg) and Vitellogenin Receptor (VgR) genes play important regulatory roles in the ovarian development of a few wasp species, but little is known about how these two genes work within O. kuvanae. Therefore, we observed their oviposition traits, characterized their gene structure, and clarified the function of Vg and VgR. The results showed that continuous daily oviposition significantly reduced the daily mature eggs and offspring per female by providing a single host egg for oviposition in each experimental trial, while the proportion of female offspring reached 100%, indicating that thelytokous parthenogenesis occurred. The full-length sequences of OkVg and OkVgR were cloned and submitted to GenBank. qPCR detection revealed that the transcription levels were the highest in adults. Feeding 20-hydroxyecdysone can increase OkVg gene expression (by 2.4-fold), while feeding juvenile hormone can promote their OkVgR expression (by 2.3-fold). RNA interference significantly downregulated OkVg and OkVgR expression in adult ovaries. And dsVg significantly reduced the ovarian egg load by 45% (p < 0.05), while dsVgR caused oviduct contraction and offspring decrease. Simultaneous silencing of OkVg and OkVgR significantly reduced offspring outcomes, indicating both genes may jointly dominate oocyte development. This study provides functional evidence of molecular regulation and interaction between OkVg and its receptor genes. Full article

Human serum albumin (HSA), as a natural protein carrier, possesses excellent biocompatibility and drug binding capacity. Due to the synergistic effects of the enhanced permeability and retention (EPR) effect and Gp60/SPARC-mediated active targeting, this drug carrier demonstrates favorable tumor selectivity and can be enriched in tumor tissues to achieve long-term therapeutic effects. Particularly, HSA undergoes pH-dependent recycling through the neonatal Fc receptor (FcRn), which significantly prolongs its half-life and enhances its feasibility as a drug delivery platform. In practical clinical applications, the regulation of HSA release rates requires multiple strategies to work synergistically. Additionally, the targeting efficiency of delivery systems due to tumor heterogeneity remains a major bottleneck limiting its universality. This article systematically reviews the unique advantages, clinical applications, challenges, and future perspectives of HSA as a prodrug carrier in tumor therapy. Full article

Soybean rust caused by the fungus Phakopsora pachyrhizi threatens global soybean production, causing yield losses of up to 80%. Race-specific Rpp genes provide short-term resistance due to pathogen variability, whereas partial resistance (PR) offers durable, broad-spectrum protection, though its genetic basis remains unclear. This study aimed to identify genomic regions and candidate genes underlying PR using the Fixed and Random Model Circulating Probability Unification (FarmCPU) genome-wide association study (GWAS) and machine learning (ML) methods, Random Forest (RF) and Support Vector Regression (SVR). A panel of 312 soybean accessions was evaluated under natural infection across six Ugandan environments. Rust index (RI), derived from rust severity and sporulation level, was used to estimate heritability (H²) and rank genotypes through Best Linear Unbiased Predictions (BLUPs), while Best Linear Unbiased Estimators (BLUEs) supported GWAS input. After quality control, 8272 SNPs were analyzed within a ±60 kb linkage disequilibrium (LD) window. Multi-environmental Analysis (MEA) of RI showed significant genetic effects (p < 0.01); H² = 0.57–0.68. Sixty-one loci were detected: six by FarmCPU, 15 by RF, and 41 by SVR. Key genes included Glyma.01G128100 (a WRKY transcription factor) and Glyma. 13G228000, receptor-like kinase) and Glyma.20G173100 (WD40-domain regulator). Integrating ML with GWAS improved locus detection, confirming the polygenic nature of PR and supporting the use of genomic selection and locus pyramiding for durable rust resistance. Full article

The H5N1 subtype of highly pathogenic avian influenza (HPAI) poses a major zoonotic threat due to its high fatality rate and capacity for cross species transmission. In early 2025, Argentina detected a novel triple reassortant A(H5N1) virus in Chaco Province, combining Eurasian, North American, and South American lineage segments. Genomic analyses of subsequent outbreaks in Buenos Aires and Entre Ríos confirmed persistence of this reassortant and additional HA substitutions (T204K, P251S) potentially linked to increased mammalian receptor affinity. Although PB2 sequences lacked canonical mammalian-adaptive markers (E627K, Q591K, D701N), all contained I292M, a mutation associated with human adaptation. Phylogenetic analyses revealed distinct genotypes and increasing divergence. These findings indicate ongoing viral evolution and adaptation within Argentina, emphasizing the urgent need for sustained genomic surveillance, timely data sharing, and integrated One Health strategies to mitigate zoonotic and socioeconomic risks associated with H5N1 spread in South America. Full article

Uridine diphosphate glucuronosyltransferases (UGTs) are critical phase II detoxification enzymes; however, their mutational landscape and protective roles against chemical carcinogenesis in hepatocellular carcinoma (HCC) remain poorly defined. Here, targeted sequencing of ten liver-enriched UGT genes in 38 paired tissues from a Chinese HCC cohort revealed striking mutation frequencies in UGT2B15 (44.74%), UGT2B10 (36.84%), and UGT2B17 (26.32%). This genomic instability was accompanied by a profound downregulation of UGT2B15 mRNA (9.02-fold decrease, p < 0.001) and protein levels (Z-score = 2.32, p = 0.0093) in tumors, with higher UGT2B15 expression correlating with improved overall survival in TCGA cohorts (HR = 1.724, p = 0.012). Mechanistically, we identified the androgen receptor (AR) as a direct transcriptional regulator of UGT2B15 and UGT2B17, with dihydrotestosterone (DHT) inducing dose-dependent increases in their expression, thereby linking endocrine signaling to hepatic detoxification. Transcriptomic profiling following UGT2B15 knockdown in HCC cells revealed a significant enrichment in chemical carcinogenesis-related pathways. Crucially, UGT2B15 deficiency severely exacerbated carbon tetrachloride (CCl₄)- and ethanol-induced hepatotoxicity both in vitro and in vivo. Our study uncovers a profound impairment of UGT-mediated detoxification in HCC and establishes the AR–UGT2B15 axis as a critical barrier against chemical-induced liver injury, highlighting its potential as a chemopreventive target in carcinogen-exposed populations. Full article

Background and Objectives: Diazepam, a GABA_A receptor agonist with sympatholytic properties, is sometimes co-administered with antiarrhythmic agents in the emergency management of atrial fibrillation (AF), yet evidence supporting this practice is remarkably limited. Given the established role of sympathetic activation in the initiation and maintenance of AF, we investigated whether adjunctive diazepam influences treatment outcomes. Materials and Methods: This single-centre retrospective cohort study included 72 hemodynamically stable patients presenting with AF to the emergency department of University Hospital Centre Split, Croatia. Patients were stratified by treatment strategy into a rhythm control group (n = 33, receiving any Class IC/III antiarrhythmic) and a rate control only group (n = 39, beta-blockers and/or digoxin). Diazepam was administered orally at the physician’s discretion (median dose 5 mg). Primary outcomes were rhythm conversion and achievement of a heart rate < 110 bpm. Secondary outcomes included changes in heart rate, blood pressure, and time to therapeutic goal. Results: Diazepam was administered to 32 patients (44.4%). In the rate control stratum, spontaneous rhythm conversion was significantly higher with diazepam (40.0% vs. 9.5%; OR 6.33, 95% CI 1.06–37.78, p = 0.046), corresponding to a model-predicted increase in conversion probability from 8% to 33%. This effect was absent in the rhythm control group (64.3% vs. 64.7%; OR 0.98, p = 1.000). Diazepam increased the odds of achieving HR < 110 bpm by 3.46-fold (95% CrI 0.63–23.1, posterior probability of benefit 92%) in the rate control group. Diazepam-treated patients in the rate control group had longer median time to therapeutic goal (4.2 vs. 2.8 h, p = 0.005). In the rhythm control group, diazepam was associated with reduced variability in diastolic blood pressure response (p = 0.006). Conclusions: Adjunctive diazepam was associated with a significantly higher rate of spontaneous rhythm conversion in AF patients receiving rate control therapy only, consistent with sympatholysis removing a key factor sustaining the arrhythmia. This effect was not observed when Class IC/III antiarrhythmics were co-administered, suggesting that diazepam’s benefit is context-dependent. These hypothesis-generating findings warrant prospective validation, with attention to thromboembolic risk in patients who convert unexpectedly. Full article

Ovarian cancer remains the most lethal gynecologic malignancy, with the majority of patients presenting at advanced stages and exhibiting poor long-term survival. High-grade serous carcinoma (HGSC), the predominant subtype, likely originates from fallopian tube epithelial cells (FTECs), whose biology is strongly influenced by hormonal signaling. Progesterone receptor (PR) expression, particularly of the PR-B isoform, is associated with improved prognosis in HGSC; however, the isoform-specific molecular mechanisms in precancerous FTECs remain unclear. This study investigated the distinct biological and transcriptomic effects of PR-A and PR-B in p53- and Rb-defective FE25 FTEC-derived cells. Stable overexpression of PR-A suppressed cell proliferation, enhanced apoptosis, and induced robust senescence, whereas PR-B promoted proliferation and activated JNK/c-Jun signaling. Upon progesterone (P4) treatment, both isoforms mediated cell-cycle arrest and apoptosis, with PR-A exhibiting stronger Sub-G1 induction. PR-A and PR-B differentially regulated cell-cycle inhibitors, senescence markers, and downstream pathways, including the PI3K–Akt and MAPK pathways, while RNA sequencing analyses revealed broader P4-induced transcriptomic changes in PR-B than in PR-A, involving immune, angiogenic, and proliferative programs. Collectively, these findings demonstrate that PR-A and PR-B exert distinct yet complementary regulatory roles in FTEC biology and progesterone responsiveness. The observed PR isoform-dependent effects in FE25 cells should be interpreted as context-specific mechanistic insights rather than direct predictors of clinical prognosis or treatment response. Full article

Background/Objectives: Calcium–phosphorus metabolism is critical for skeletal development in weaned piglets. This study evaluated the effects of dietary 25-hydroxyvitamin D₃ (25-OH-VD₃) in combination with phytase and probiotics on mineral metabolism, bone development, and related molecular mechanisms in weaned piglets. Methods: Sixty 28-day-old weaned piglets (7.1 ± 1.30 kg) were randomly assigned to four dietary treatments for 31 days (including 3 days of acclimation): CON (basal diet + 50 µg/kg 25-OH-VD₃), HI (CON + 50 mg/kg phytase), CY (CON +10 mg/kg probiotics), HICY (CON + 50 mg/kg phytase + 10 mg/kg probiotics). Apparent calcium digestibility, serum biochemical indices, bone mineral density (BMD), and mRNA and protein expression of calcium–phosphorus transport- and metabolism-related genes in jejunal mucosa and kidney were assessed. Results: Compared with CON, piglets in the HI, CY, and HICY groups showed higher apparent calcium digestibility (p < 0.05). Serum transforming growth factor-β was elevated in CY and HICY (p < 0.05). HI enhanced metatarsal and toe BMD (p < 0.05) and upregulated jejunal solute carrier family 34, member 2 (SLC34A2) and SLC34A3 mRNA expression (p < 0.05). In contrast, HICY reduced mRNA expression of transient receptor potential cation channel subfamily V member 6 and calcium-binding protein D28k, as well as of calcium-binding protein D9k and cytochrome P450 27B1 in the kidney (p < 0.05). Renal calcium-sensing receptor protein abundance increased in CY (p < 0.05). Conclusions: Supplementation of 25-OH-VD₃ with phytase and/or probiotics improved calcium utilization and modulated key transport pathways, contributing to enhanced bone development in weaned piglets. These findings highlight coordinated nutritional regulation of mineral metabolism during early post-weaning growth. Full article