Sci Rep. 2025 May 8;15(1):15979. doi: 10.1038/s41598-025-99903-y.

ABSTRACT

Visually impaired individuals suffer many problems in handling their everyday activities like road crossing, writing, finding an object, reading, and so on. However, many navigation methods are available, and efficient object detection (OD) methods for visually impaired people (VIP) need to be improved. OD is the most crucial contribution of computer vision (CV) and plays an important part in recognizing and finding objects in the image. The aged and visually challenged people can identify different objects accurately under some constraint features like scaled, occlusion, illuminated, and blurred nature in different real world. A considerable number of studies are performed in the domain of real-time object recognition using deep learning (DL). The DL-based methods remove the features autonomously and classify and detect the objects. This paper proposes a novel Object Detection Model for Visually Impaired Individuals with a Metaheuristic Optimization Algorithm (ODMVII-MOA) technique. The proposed ODMVII-MOA technique aims to improve OD methods in real-time with advanced techniques to detect and recognize objects for disabled people. At first, the image pre-processing stage applies the Weiner filter (WF) method to enhance image quality by eliminating the unwanted noise from the data. Furthermore, the RetinaNet technique is utilized for the OD process to recognize and locate objects within an image. Besides, the proposed ODMVII-MOA method employs the EfficientNetB0 method for the feature extraction process. For the classification process, the LSTM-AE method is employed. Finally, the Dandelion Optimizer (DO) method adjusts the hyperparameter range of the LSTM-AE method optimally and results in better performance of classification. The experimental validation of the ODMVII-MOA model is verified under the indoor OD dataset and the outcomes are determined regarding different measures. The comparison study of the ODMVII-MOA model portrayed a superior accuracy value of 99.69% over existing techniques.

PMID:40341297 | DOI:10.1038/s41598-025-99903-y

NPJ Digit Med. 2025 May 8;8(1):260. doi: 10.1038/s41746-025-01654-7.

ABSTRACT

Speech dysarthria is a key symptom of neurological conditions like ALS, yet existing AI models designed to analyze it from audio signal rely on handcrafted features with limited inference performance. Deep learning approaches improve accuracy but lack interpretability. We propose an attention-based deep learning AI model to assess dysarthria severity based on listener effort ratings. Using 2,102 recordings from 125 participants, rated by three speech-language pathologists on a 100-point scale, we trained models directly from recordings collected remotely. Our best model achieved R2 of 0.92 and RMSE of 6.78. Attention-based interpretability identified key phonemes, such as vowel sounds influenced by 'r' (e.g., "car," "more"), and isolated inspiration sounds as markers of speech deterioration. This model enhances precision in dysarthria assessment while maintaining clinical interpretability. By improving sensitivity to subtle speech changes, it offers a valuable tool for research and patient care in ALS and other neurological disorders.

PMID:40341287 | DOI:10.1038/s41746-025-01654-7

BMC Pulm Med. 2025 May 8;25(1):221. doi: 10.1186/s12890-025-03689-8.

ABSTRACT

BACKGROUND: The antifibrotic therapies, pirfenidone and nintedanib, have been approved since 2014 for idiopathic pulmonary fibrosis (IPF), but in the United States only a quarter of people living with IPF have ever been exposed to an antifibrotic. Understanding the burden and consequences of the disease and its treatment from the perspective of people living with IPF may facilitate improved education and outreach for them and their providers.

METHODS: Qualitative interviews with people living with IPF explored perspectives on the diagnosis and management of IPF. Transcripts were analyzed to derive themes and topics, and illustrative quotes were selected for presentation. Data were developed into a 74-item on-line survey taken by additional people living with IPF. Quantitative survey data were analyzed with 95% confidence intervals and Z tests.

RESULTS: Sixteen people living with IPF underwent qualitative interviews. Direct quotes were used to derive and support themes, and survey stimuli are presented. Ninety additional people living with IPF responded to the on-line survey. 52% of survey participants were male, 54% used supplemental oxygen, and 34% had never been exposed to an antifibrotic. Top sources of information about their IPF diagnosis were their healthcare provider, the internet, and support groups. Most participants had one or more of shortness of breath, fatigue, or cough and over 40% described these symptoms as very burdensome. The most common reason for not starting an antifibrotic was, "I am waiting to start treatment until my symptoms worsen." For those treated with antifibrotics, (78%) agreed with a statement that their antifibrotic gives them hope even though around 90% had at least one side effect.

CONCLUSIONS: Most individuals living with IPF experienced significant challenges due to their disease and its treatment, that substantially impacted their quality of life. A better understanding of these challenges can facilitate patient-centered and shared decision-making, ultimately enhancing outcomes and satisfaction for people living with IPF.

PMID:40340670 | DOI:10.1186/s12890-025-03689-8

Nat Commun. 2025 May 9;16(1):4313. doi: 10.1038/s41467-025-59569-6.

ABSTRACT

The K29/K48-linked ubiquitination generated by the cooperative catalysis of E3 ligase Ufd4 and Ubr1 is an enhanced protein degradation signal, in which Ufd4 is responsible for introducing K29-linked ubiquitination to K48-linked ubiquitin chains to augment polyubiquitination. How HECT-E3 ligase Ufd4 mediates the ubiquitination event remains unclear. Here, we biochemically determine that Ufd4 preferentially catalyses K29-linked ubiquitination on K48-linked ubiquitin chains to generate K29/K48-branched ubiquitin chains and capture structural snapshots of Ub transfer cascades for Ufd4-mediated ubiquitination. The N-terminal ARM region and HECT domain C-lobe of Ufd4 are identified and characterized as key structural elements that together recruit K48-linked diUb and orient Lys29 of its proximal Ub to the active cysteine of Ufd4 for K29-linked branched ubiquitination. These structures not only provide mechanistic insights into the architecture of the Ufd4 complex but also provide structural visualization of branched ubiquitin chain formation by a HECT-type E3 ligase.

PMID:40341121 | DOI:10.1038/s41467-025-59569-6

J Nucl Med. 2025 May 8:jnumed.124.267660. doi: 10.2967/jnumed.124.267660. Online ahead of print.

ABSTRACT

The study of the human phenome is essential for understanding the complexities of wellness and disease and their transitions, with molecular imaging being a vital tool in this exploration. Molecular imaging embodies the 4 principles of human phenomics: precise measurement, accurate calculation or analysis, well-controlled manipulation or intervention, and innovative invention or creation. Its application has significantly enhanced the precision, individualization, and effectiveness of medical interventions. This article provides an overview of molecular imaging's technologic advancements and presents the potential use of molecular imaging in human phenomics and precision medicine. The integration of molecular imaging with multiomics data and artificial intelligence has the potential to transform health care, promoting proactive and preventive strategies. This evolving approach promises to deepen our understanding of the human phenome, lead to preclinical diagnostics and treatments, and establish quantitative frameworks for precision health management.

PMID:40341093 | DOI:10.2967/jnumed.124.267660

Genome Biol. 2025 May 8;26(1):119. doi: 10.1186/s13059-025-03590-x.

ABSTRACT

BACKGROUND: Cell-free RNAs (cfRNAs) can be detected in biofluids and have emerged as valuable disease biomarkers. Accurate identification of the fragmented cfRNA signals, especially those originating from pathological cells, is crucial for understanding their biological functions and clinical value. However, many challenges still need to be addressed for their application, including developing specific analysis methods and translating cfRNA fragments with biological support into clinical applications.

RESULTS: We present cfPeak, a novel method combining statistics and machine learning models to detect the fragmented cfRNA signals effectively. When test in real and artificial cfRNA sequencing (cfRNA-seq) data, cfPeak shows an improved performance compared with other applicable methods. We reveal that narrow cfRNA peaks preferentially overlap with protein binding sites, vesicle-sorting sites, structural sites, and novel small non-coding RNAs (sncRNAs). When applied in clinical cohorts, cfPeak identified cfRNA peaks in patients' plasma that enable cancer detection and are informative of cancer types and metastasis.

CONCLUSIONS: Our study fills the gap in the current small cfRNA-seq analysis at fragment-scale and builds a bridge to the scientific discovery in cfRNA fragmentomics. We demonstrate the significance of finding low abundant tissue-derived signals in small cfRNA and prove the feasibility for application in liquid biopsy.

PMID:40340952 | DOI:10.1186/s13059-025-03590-x

BMC Plant Biol. 2025 May 8;25(1):604. doi: 10.1186/s12870-025-06595-7.

ABSTRACT

BACKGROUND: Rice is a critical global food source, but it faces challenges due to nutritional deficiencies and the pressures of a growing population. Understanding the molecular mechanisms and protein functions in rice seed development is essential to improve yield and grain quality. However, there is still a significant knowledge gap regarding the key proteins and their interactions that govern rice seed development. Protein-protein interaction (PPI) analysis is a powerful tool for studying developmental processes like seed development, though its potential in rice research is yet to be fully realized. With the aim of unraveling the protein interaction landscape associated with rice seed development, this systems biology study conducted a PPI network-based analysis. Using a list of known seed development proteins from the Gene Ontology (GO) knowledgebase and literature, novel candidate proteins for seed development were predicted using an ensemble of network-based algorithms, including Majority Voting, Hishigaki Algorithm, Functional Flow, and Random Walk with Restart, which were selected based on their popularity and usability. The predictions were validated using enrichment analysis and cross-checked with independent transcriptomic analysis results. The rice seed development sub-network was further analyzed for community and hub detection.

RESULTS: The study predicted 196 new proteins linked to rice seed development and identified 14 sub-modules within the network, each representing different developmental pathways, such as endosperm development and seed growth regulation. Of these, 17 proteins were identified as intra-modular hubs and 6 as inter-modular hubs. Notably, the protein SDH1 emerged as a dual hub, acting as both an intra-modular and inter-modular hub, highlighting its importance in seed development PPI network stability.

CONCLUSIONS: These findings, including the identified hub proteins and sub-modules, provide a better understanding of the PPI interaction landscape governing seed development in rice. This information is useful for achieving a systems biology understanding of seed development. This study implements an ensemble of algorithms for the analysis and showcases how systems biology techniques can be applied in developmental biology.

PMID:40340735 | DOI:10.1186/s12870-025-06595-7

J Clin Endocrinol Metab. 2025 May 8:dgaf276. doi: 10.1210/clinem/dgaf276. Online ahead of print.

ABSTRACT

BACKGROUND: Observational studies have shown association between polycystic ovary syndrome (PCOS) and asthma-related traits. However, whether this association is genetically driven or arises from observational biases remains unclear.

METHODS: This study integrated data from 10,074 PCOS cases and asthma-related traits obtained from UK Biobank and FinnGen cohorts. Global and local genetic architectures were examined using pleiotropic analysis under the composite null hypothesis, Functional Mapping and Annotation of Genetic Associations, and fine-mapping credible set analysis. Drug database mining was employed to identify pleiotropic genes as potential therapeutic targets. Tissue and cell enrichment analyses were conducted to uncover shared biological mechanisms.

RESULTS: We identified 3 novel significant genetic loci for asthma subtypes (2 for allergic asthma and 1 for childhood asthma). A positive overall genetic correlation between PCOS and asthma-related traits was observed. We discovered 5 pleiotropic causal regions encompassing 13 genes, with ERBB3 emerging as a potential central gene contributing to the shared pathophysiology of PCOS and asthma-related traits. Additionally, drug repositioning analysis suggested anakinra and artenimol as potential therapeutic candidates for PCOS and asthma comorbidity. Linkage disequilibrium score for the specific expression of genes analysis, along with transcriptome-wide association study, further identified gene expression patterns at the tissue/cell level in hypothalamo-pituitary, exocrine/endocrine, respiratory, and urogenital systems.

CONCLUSIONS: Our findings provide novel insights into the genetic basis and biological processes underlying the association between PCOS and asthma-related traits, warranting evaluation of whether PCOS-specific asthma risk assessment could improve clinical outcomes.

PMID:40339110 | DOI:10.1210/clinem/dgaf276

J Clin Invest. 2025 May 8:e181394. doi: 10.1172/JCI181394. Online ahead of print.

ABSTRACT

The activated JAK2/STAT pathway is characteristic of myeloproliferative neoplasms (MPNs). Pleckstrin-2 (PLEK2) signalosome is downstream of the JAK2/STAT5 pathway and plays an important role in MPN development. The detailed molecular composition of this signalosome is unclear. Here, we revealed peptidylprolyl isomerase-like 2 (PPIL2) as a critical component of the complex in regulating human and murine erythropoiesis. PPIL2 was a direct target of STAT5 and was upregulated in MPN patients and a Jak2V617F MPN mouse model. Mechanistically, PPIL2 interacted with and catalyzed p53 polyubiquitination and proteasome-mediated degradation to promote cell growth. Ppil2 deficiency, or inhibition by cyclosporin A, led to a marked upregulation of p53 in vivo and ameliorated myeloproliferative phenotypes in Jak2V617F mice. Cyclosporin A also markedly reduced JAK2 mutated erythroid and myeloid proliferation in an induced pluripotent stem cell-derived human bone marrow organoid model. Our findings revealed PPIL2 as a critical component of the PLEK2 signalosome in driving MPN pathogenesis through negatively regulating p53, thus providing a target and an opportunity for drug repurposing by using cyclosporin A to treat MPNs.

PMID:40338661 | DOI:10.1172/JCI181394

Hematol Transfus Cell Ther. 2025 May 7;47(2):103759. doi: 10.1016/j.htct.2025.103759. Online ahead of print.

ABSTRACT

OBJECTIVE: This study aimed to determine the frequency of genetic alterations as deletions and duplications in cytochrome P450 (CYP450) and glutathione S-transferases (GST) genes, as well as to investigate whether there is a relationship between these alterations and neutrophilic hematologic recovery in adult patients diagnosed with acute myeloid leukemia.

METHOD: DNA samples from 70 patients diagnosed with acute myeloid leukemia were evaluated using the Multiplex Ligation-dependent Probe Amplification technique. The presence or absence of polymorphisms was compared regarding the time to neutrophilic recovery (neutrophil count ≥1.0 × 109/L) using Kaplan-Meier curves, with the comparison between the curves being performed using the non-parametric log-rank test.

RESULTS: The median age of the participants was 57 years, with a higher proportion of females (57.2%) and white individuals (61.4%)'. A total of 76 polymorphisms (CYP450 + GST) were identified, comprising 38 deletions and 38 duplications. Kaplan-Meier curves revealed that the neutrophilic recovery time was longer for the group with polymorphisms (p-value = 0.0056).

CONCLUSION: The study demonstrated that CYP450 and GST genes are polymorphic, and these polymorphisms may lead to longer neutrophilic recovery after induction treatment of acute myeloid leukemia remission.

PMID:40339533 | DOI:10.1016/j.htct.2025.103759

Early Hum Dev. 2025 May 1;206:106272. doi: 10.1016/j.earlhumdev.2025.106272. Online ahead of print.

ABSTRACT

Physical activity (PA) during pregnancy may have a positive effect on the fetal cardiac maturation which is reflected in a decreasing resting heart rate and increasing heart rate variability (HRV). Different types of PA, for example during leisure or work time, have differential effects on HRV; however, this relationship has not yet been investigated in pregnancy. In our work, we related different types of PA during pregnancy with maternal and fetal HRV. We assessed the levels of PA in 95 pregnant women between 28 and 32 weeks of gestational age using the Baecke Physical Activity Questionnaire. Maternal and fetal heart rate and HRV were extracted from magnetocardiography recordings at rest, and maternal anthropometric and metabolic parameters were measured, such as fasting glucose and insulin levels, body mass index, and blood pressure. Pearson correlations were calculated between HRV, PA, and maternal parameters. Principal component analysis and generalized linear models were implemented to further investigate these relationships. Our findings indicate that habitual physical activity, whether during leisure or work, has no significant effect on maternal or fetal HRV at rest. However, leisure-time physical activity, unlike work-related activity, is associated with improved maternal insulin sensitivity. Additionally, our exploratory analyses revealed that lower HRV in both the mother and the fetus is associated with poorer maternal metabolic health quantified through higher fasting insulin levels, triglycerides, and adiposity. Finally, male fetuses showed higher HRV compared to females, highlighting the difference in cardiac development between the two biological sexes.

PMID:40339304 | DOI:10.1016/j.earlhumdev.2025.106272

J Cyst Fibros. 2025 May 7:S1569-1993(25)00768-4. doi: 10.1016/j.jcf.2025.04.002. Online ahead of print.

ABSTRACT

BACKGROUND: Pulmonary hypertension (PH) is an important, life-limiting co-morbidity in cystic fibrosis (CF), where multiple mechanisms such as hypoxia, inflammation and primary CF-transmembrane regulator (CFTR) dysfunction may affect vascular integrity. We aimed to characterize the structural impact of vascular wall changes in the pulmonary microcirculation, to uncover the potential need for therapeutic strategies targeting vascular disease.

METHODS: End-stage inflated CF (n=6), and control (n=4) lungs were processed to lung cores (2.8cm³) and scanned with micro-computed tomography (resolution: 8.5µm). The diameter and number of distal pulmonary arteries (dPA), distal airways (DA) and open terminal bronchioles (TB) were measured on 3D models (n= 2 cores/lobe) and compared per generation and within pairs. Morphometric assessment was paired with histological analysis (n= 1/lobe) to assess tissue morphology, collagen and connective tissue components.

RESULTS: dPA in CF were narrowed and disappeared in the last generations of dichotomous branching, resulting in a decreased total diameter per generation. While narrowing was already present where TB remained open, dPA disappearance was only present where no TB were left. dPA narrowing increased when DA collapsed. Histologically, fibrotic dPA changes were present in areas without distal airway disease.

CONCLUSION: We showed for the first time the presence of dPA lumen narrowing and disappearance with fibrotic vascular wall changes in end-stage CF. Narrowing was present diffusely and fibrosis was also present in areas without airway disease. These findings suggest that vascular dysfunction in CF may not solely be secondary to hypoxic vasoconstriction and inflammation but may represent a distinct pathophysiological process related to CFTR dysfunction in the endothelium, warranting further study.

PMID:40340199 | DOI:10.1016/j.jcf.2025.04.002

Respir Med. 2025 May 6:108136. doi: 10.1016/j.rmed.2025.108136. Online ahead of print.

ABSTRACT

BACKGROUND: Non-cystic fibrosis bronchiectasis (NCFB) is often complicated by chronic Pseudomonas aeruginosa infection. Inhaled antibiotics, such as tobramycin, have been explored for their efficacy in managing these infections, but their efficacy and safety in NCFB remains uncertain.

METHODS: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to assess the efficacy and safety of inhaled tobramycin in NCFB patients. PubMed, EMBASE, Cochrane Library, and ISI Web of Science databases were searched up to June 2024 using predefined keywords. Studies comparing inhaled tobramycin versus placebo were included if they reported outcomes related to P. aeruginosa eradication, sputum density, exacerbations, hospital admissions, and adverse events.

RESULTS: Nine RCTs involving 772 patients met the inclusion criteria. Inhaled tobramycin significantly increased P. aeruginosa eradication rates compared to placebo (I2=22.0%, P=0.255; RR 2.422, 95% CI 1.570 to 3.738, P<0.001). There was a marked reduction in hospital admissions (I2=27.9%, P=0.250; WMD -0.523, 95% CI -0.879 to -0.167, P=0.004) but no significant difference in exacerbation rates (I2=31.9%, P=0.196; RR 0.837, 95% CI 0.519 to 1.349, P=0.464). Adverse events leading to trial discontinuation were higher in the tobramycin group (I2=0.0%, P=0.634; RR 1.968, 95% CI 1.197 to 3.236, P=0.008).

CONCLUSIONS: Inhaled tobramycin therapy demonstrated efficacy in eradicating P. aeruginosa and reducing hospital admissions in patients with NCFB. However, no significant impact on exacerbation rates was observed, and the higher incidence of adverse events necessitates careful consideration in clinical practice.

PMID:40339664 | DOI:10.1016/j.rmed.2025.108136

J Biotechnol. 2025 May 6:S0168-1656(25)00109-9. doi: 10.1016/j.jbiotec.2025.04.024. Online ahead of print.

ABSTRACT

The single-step biotransformation of the natural compound piperine into a known dual inhibitor of monoamine oxidase B (MAO-B) and catechol-O-methyltransferase (COMT), was achieved by cytochrome P450 BM3 wild-type and the D251G/Q307H double mutant. This compound is used for research in neurodegenerative disorders, such as Parkinson's disease, and its value in the market is ~14,000 €/g. Currently, it is produced by chemical synthesis requiring incubation of piperine with boron tribromide (BBr3) in dichloromethane with yield of product not exceeding 55% and using tedious and long procedure for its production and isolation. The P450 D251G/Q307H double mutant exhibited a 3-fold increase in catalytic efficiency compared to the wild-type enzyme, achieving high conversion (51.6% of conversion in 15minutes) under mild, environmentally friendly conditions. The yield of production was 0.01mg of the inhibitor in 1mL of reaction in 15minutes at 28°C using the purified enzyme. Moreover, biological assays demonstrated that the resulting compound has a novel and stronger antioxidant and antimicrobial activities, respectively, when compared to piperine. The data further demonstrates the broader potential of engineered enzymes as versatile and sustainable tools in industrial biotechnology, offering an efficient platform for the modification of natural compounds to produce bioactive molecules.

PMID:40339650 | DOI:10.1016/j.jbiotec.2025.04.024

Cell. 2025 May 5:S0092-8674(25)00353-8. doi: 10.1016/j.cell.2025.03.035. Online ahead of print.

ABSTRACT

The emergence of SARS-CoV in 2002 and SARS-CoV-2 in 2019 led to increased sampling of sarbecoviruses circulating in horseshoe bats. Employing phylogenetic inference while accounting for recombination of bat sarbecoviruses, we find that the closest-inferred bat virus ancestors of SARS-CoV and SARS-CoV-2 existed less than a decade prior to their emergence in humans. Phylogeographic analyses show bat sarbecoviruses traveled at rates approximating their horseshoe bat hosts and circulated in Asia for millennia. We find that the direct ancestors of SARS-CoV and SARS-CoV-2 are unlikely to have reached their respective sites of emergence via dispersal in the bat reservoir alone, supporting interactions with intermediate hosts through wildlife trade playing a role in zoonotic spillover. These results can guide future sampling efforts and demonstrate that viral genomic regions extremely closely related to SARS-CoV and SARS-CoV-2 were circulating in horseshoe bats, confirming their importance as the reservoir species for SARS viruses.

PMID:40339581 | DOI:10.1016/j.cell.2025.03.035

Cell Syst. 2025 May 5:101292. doi: 10.1016/j.cels.2025.101292. Online ahead of print.

ABSTRACT

The arginine dihydrolase pathway (arc operon) provides a metabolic niche by transforming arginine into metabolic byproducts. We investigate the role of the arc operon in probiotic Escherichia coli Nissle 1917 on human gut community assembly and health-relevant metabolite profiles. By stabilizing environmental pH, the arc operon reduces variability in community composition in response to pH perturbations and frequently enhances butyrate production in synthetic communities. We use a tailored machine learning model for microbiomes to predict community assembly in response to variation in initial media pH and arc operon activity. This model uncovers the pH- and arc operon-dependent interactions shaping community assembly. Human gut species display altered colonization dynamics in response to the arc operon in the murine gut. In sum, our framework to quantify the contribution of a specific pathway to microbial community assembly and metabolite production can reveal new engineering strategies. A record of this paper's transparent peer review process is included in the supplemental information.

PMID:40339579 | DOI:10.1016/j.cels.2025.101292

Dev Cell. 2025 May 2:S1534-5807(25)00250-3. doi: 10.1016/j.devcel.2025.04.012. Online ahead of print.

ABSTRACT

The lymphatic vasculature comprises lymphatic capillaries and collecting vessels. To support lymphatic development, lymphatic endothelial cells (LECs) utilize nutrients to fuel lymphangiogenic processes. Meanwhile, LECs maintain constant prospero homeobox 1 (PROX1) expression critical for lymphatic specification. However, molecular mechanisms orchestrating nutrient metabolism while sustaining PROX1 levels in LECs remain unclear. Here, we show that loss of RAPTOR, an indispensable mechanistic target of rapamycin complex 1 (mTORC1) component, downregulates PROX1 and impairs lymphatic capillary growth and differentiation of collecting lymphatics in mice. Mechanistically, mTORC1 inhibition in mouse and human LECs causes Myc reduction, which decreases hexokinase 2 (HK2) and glutaminase (GLS), inhibiting glycolysis and glutaminolysis. Myc or HK2/GLS ablation impedes lymphatic capillary and collecting vessel formation. Interestingly, mTORC1 regulation of PROX1 is independent of Myc-HK2/GLS signaling. Moreover, genetic interaction analysis indicates that Myc and PROX1 play crucial roles in mTORC1-regulated lymphatic development. Collectively, our findings identify mTORC1 as a key regulator of metabolic programs and PROX1 expression during lymphangiogenesis.

PMID:40339577 | DOI:10.1016/j.devcel.2025.04.012