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Field phenotyping of a recently established NAM population for stem rust resistance, combined with high-density genotyping, enabled the identification of novel sources of stem rust resistance in Italian ryegrass. Stem rust, caused by Puccinia graminis ssp. graminicola, is a major disease affecting the outcrossing species Italian ryegrass (Lolium multiflorum Lam.) and leading to substantial reductions in seed yield. Until now, knowledge on the genetic control of stem rust resistance in Italian ryegrass has been limited to a few quantitative trait loci identified in biparental mapping populations. To discover novel resistance sources for use in breeding programs, appropriate plant populations, reliable phenotyping methods and advanced genomic tools are essential. In this study, we utilized a previously established F2 nested association mapping (NAM) population comprising 708 individuals derived from 24 founder plants, exhibiting high variation in stem rust resistance. Phenotypic evaluation was conducted under natural inoculation in three location-by-year combinations. By integrating reduced-representation sequencing of the NAM population with whole genome sequencing of the founder plants, we identified 3,199,253 SNP markers for association mapping. The high SNP marker density, together with the strong detection power of the NAM population, enabled the identification of four novel candidate genes. Two of these genes, located on chromosomes 6 and 7, encode receptor-like serine/threonine kinases that are known to play a role in stem rust resistance in other crops. Within the serine/threonine kinase gene Chr7.32208, two superior haplotypes were identified that can be directly implemented as selection criteria in breeding programs. The novel stem rust resistance candidate genes reported here provide promising targets for functional validation and the improvement of stem rust resistance in Italian ryegrass breeding.

Biological invasions offer large-scale experiments for examining rapid evolution and testing the predictability of adaptive change. Assessing the repeatability of such adaptive responses, however, requires replicated introductions that share similar demographic and environmental contexts. Single introduction events are common during biological invasion, but replicated secondary introductions from a shared source are rare. Here, we take advantage of a unique study system involving the introduced rusa deer (Cervus timorensis) to investigate whether synchronous secondary introductions from a shared bridgehead population show similar evolutionary trajectories. We utilised 5298 DArTSeq Single Nucleotide Polymorphisms (SNPs) from a bridgehead population and two secondary populations to estimate genetic diversity, characterise population structure and detect SNPs putatively under selection. We found an apparent reduction in genetic diversity across serial introductions, consistent with strong founder effects. Population genetic analyses revealed two genetic clusters, indicating strong differentiation and independent evolutionary trajectories between secondary populations. A genome-wide scan using BayPass identified outlier SNPs potentially involved in adaptive responses and some evidence of parallel selection, likely driven by common environmental pressures. We found candidate genes linked to the outlier loci that were associated with functions consistent with adaptive mechanisms. This study highlights that repeated introductions from a common source can further reduce genetic diversity and increase population differentiation, yet still produce parallel adaptive responses under similar environmental conditions.

Extended-spectrum β-lactamase (ESBL)-producing Escherichia coli (E. coli), a bacterium resistant to most β-lactam antibiotics, is a critical clinical global health concern, posing significant health risks to humans and animals including giant pandas. The Chengdu Research Base of Giant Panda Breeding (CRBGP) has the world's largest captive population of giant pandas. This study aimed to investigate the prevalence, antibiotic resistance characteristics, and molecular epidemiology of ESBL-producing E. coli among captive giant pandas at the CRBGP. ESBL production was screened in 100 E. coli isolates from 100 individual giant pandas (different ages and sexes) using the Clinical and Laboratory Standards Institute (CLSI) double-disc combination test. ESBL isolates were subjected to antimicrobial susceptibility testing of 34 antibiotics using the Kirby-Bauer disk diffusion susceptibility test (K-B). Whole genome sequencing (WGS) was performed to characterize genotypes, antibiotic resistance genes (ARGs), mobile genetic elements (MGEs), and multilocus sequence typing (MLST), and the molecular epidemiology of the isolates was further investigated using MLST and the goeBURST algorithm. Twenty-nine ESBL-producing E. coli strains were identified (29.0%, 29/100), representing a marked increase from the 8% prevalence reported during 2020-2021. All 29 isolates exhibited high resistance to β-lactam antibiotics, with 100.0% resistance to amoxicillin, ampicillin, cefazolin, cefuroxime and cefotaxime. A total of 120 different ARG subtypes and 19 ESBL gene subtypes were detected; bla CTX-M-4 was the most prevalent (100.0%), followed by bla SHV-1 (96.6%), bla CTX-M-1 and bla CTX-M-3 (93.1% each). Analysis of MGEs revealed high carriage rates of IS26 (89.7%), intI1 (89.7%), and the conjugation-associated gene traA (51.7%). MLST identified 10 sequence types (STs) and one clonal complex (CC1), with ST132 as the founder. ST595 and ST973 were the most common STs (each n = 7). The prevalence of ESBL-producing E. coli in captive giant pandas at the CRBGP has risen sharply (29.0%), with high-level multidrug resistance (MDR), a large ARG repertoire, and abundant MGEs indicative of strong horizontal gene transfer (HGT) potential. The presence of shared STs with other hosts suggests potential interspecies transmission. These findings underscore the urgent need for enhanced antimicrobial stewardship and continuous One Health surveillance to protect giant pandas and the broader ecosystem.

Rare variants in SETD1A , encoding a histone H3K4 methyltransferase, are among the strongest genetic risk factors for schizophrenia. Exome sequencing (n = 3,736) revealed a population-enriched SETD1A missense variant (P596L) in the Lancaster Old Order Amish founder population, presenting a unique opportunity to elucidate variant-specific, multi-scale mechanisms. Psychiatric and cognitive phenotyping revealed nearly two-fold increased risk for bipolar disorder, accompanied by allele dose-dependent cognitive deficits in adulthood. Induced pluripotent stem cells (iPSCs) from homozygous carriers exhibited signatures of SETD1A hypofunction, including reduced proliferation and heightened susceptibility to replication stress and DNA double-strand breaks. During forebrain-directed differentiation, homozygous mutant cells displayed premature activation of neurodevelopmental transcriptional programs but impaired neural rosette formation, reduced neurite complexity, and early progenitor senescence. Multi-omic profiling revealed dysregulation of gene modules converging on replication stress pathways and neuronal regulatory networks enriched for autism and psychiatric risk genes. Pharmacologic inhibition of the H3K4 demethylase KDM5 partially rescued replication stress and neurite deficits, supporting an epigenetic mechanism and suggesting therapeutic tractability. Together, these findings link a population-enriched missense variant to disrupted chromatin regulation, genome stability, and neurodevelopmental timing, bridging human genetic risk with cellular pathophysiology.

Stathmin-2 (STMN2) is a microtubule-associated protein that plays a role in the stability of microtubules in axons of the nervous system of animals. In this study, we generated a novel zebrafish STMN2 knockout (KO) model. STMN2 is represented by two genes in the zebrafish genome: stmn2a and stmn2b. Using the CRISPR/Cas9 mutagenic system, we selected founder fish lines harboring frameshift mutations in both genes and bred these together to generate a double stmn2a and stmn2b KO model. Using these models, we observed increased developmental lethality in our double stmn2a and stmn2b KO model and impaired motor function at embryonic stages of development. Examination of the neuromuscular junction (NMJ) revealed a slight increase in the number of orphaned NMJs in trunk musculature as well as a reduction in the amplitude of miniature endplate currents in our double stmn2a and stmn2b KO model. In a final series of experiments, we show impaired ventral root axon regrowth following transection in double stmn2a and stmn2b KO zebrafish. Our findings suggest that while not essential for motor function development, loss of stmn2a and stmn2b expression results in a minor motor phenotype and impairs the ability to regenerate motor axons following injury.

RNA viruses are responsible for many zoonotic disease transmission events, and remain a global health challenge. To evade immune detection, RNA viruses suppress the numbers of immunostimulatory oligonucleotide motifs (INMs) present in their genomes. Although this is thought to occur in human immunodeficiency virus-1 (HIV-1), our bioinformatic analysis on well characterized clinical datasets, along with in vitro studies, demonstrate that HIV-1 is enriched for INMs within its transmitted/founder (T/F) population relative to non-transmitting variants. Importantly, our data suggests that within the host, there is an evolutionary genetic replacement of T/F viruses that otherwise exhibit high transmission fitness and low replicative fitness, with variants having low transmission fitness but high replicative fitness. These findings provide insights into HIV-1 transmission by studying within-host and between-host evolutionary dynamics, enabling us to identify a framework for HIV infection biology, with viral RNA playing a role in transmission and replication processes.

Oral cancer is a significant health issue in the country, accounting for one-fourth of all cases worldwide. A shortage of specialized healthcare, limited access to screening tools, and diagnostic facilities are key contributors to delayed diagnosis. Artificial Intelligence can be a promising tool for the early screening of oral cancer. However, its application in India remains underexplored and lacks systematic evaluation. A scoping review was conducted using the Arksey and O'Malley (2005) framework and the approach by Peters et al. (2015). The PRISMA framework was adopted for selecting relevant studies on AI applications for oral cancer screening in India. Studies were systematically searched in PubMed, CINAHL, Scopus, and Google Scholar. Reviewers extracted relevant data and systematically mapped them to identify strengths, weaknesses, opportunities, and threats of AI applications in oral cancer screening within India. Of the 265 identified studies, 33 were selected for final review. Various designs were used, including cross-sectional field evaluations, pilot and prospective studies, scoping and systematic reviews, narrative reviews, and experimental studies. AI methodologies demonstrated high diagnostic accuracy, with strengths in portability, scalability, and affordability in low-resource settings. Weaknesses reported were a lack of standardized data, limited digital literacy, and infrastructural gaps. AI models offer opportunities to enhance screening coverage, integrate multimodal datasets, and support personalized treatment planning. Key threats observed were data variability, lack of regulatory and ethical frameworks, and data privacy concerns. AI offers strengths in improving oral cancer screening in India through early detection and reducing inequities. Despite its promising strengths, AI faces challenges such as scalability, infrastructure gaps, and ethical issues when implemented for oral cancer screening in the Indian context. For the successful integration of AI, technological innovation, robust digital infrastructure, adequate workforce training, and regulatory guidelines are required.

The rapid pace of innovation in synthetic biology and genome engineering elicits a need to reevaluate systems of oversight to ensure that biosafety and biosecurity safeguards are keeping up. Accordingly, the regulation of nucleic acid synthesis, an enabling technology for synthetic biology and genome engineering, is a current focus of political debate in the United States. However, to develop appropriate governance that neither under- nor overregulates technological development, policy leaders must also appreciate how advances in synthetic biology and genome engineering are being employed in the interests of biosecurity to support human health, manufacturing, food security, ecosystems and the natural environment. Synthetic biology can support the development of new therapeutics and health technologies, alternative biomanufacturing methodologies, food and agricultural innovations, environmental biosensors for monitoring infectious and toxic agents, and interventions aimed at preserving and restoring our natural environment. This Perspective provides an overview of current and potential benefits of synthetic biology and genome engineering, aiming to balance the broader societal discussion of potential risks-particularly in this special issue of the journal-with potential social, economic, and environmental value to individuals and society at large.

The Early Cold Stored Platelet Transfusion Following Severe Trauma Injury Trial evaluated the safety and efficacy of cold stored platelet (CSP) transfusion in injured patients at risk of hemorrhagic shock. It was a phase II, multicenter, randomized clinical trial conducted from June 2022 to September 2023 at five US level 1 trauma centers. A total of 200 adult patients at risk of hemorrhagic shock (102 CSP, 98 standard care (SC)) were included. Median age was 34±13 years, 85% were males, and injury severity was similar between groups. The original frequentist analysis did not demonstrate a statistically significant difference in 24-hour mortality between CSP (5.9%) transfusion and SC (10.2%, p=0.28). To provide further insight into these findings, a Bayesian logistic regression outcome model with an uninformative prior was performed. To validate the findings further, a sensitivity analysis was performed in addition to analysis using a beta-binomial Bayesian model. The Bayesian logistic regression model yielded an 89.1% posterior probability that CSP transfusion reduced 24-hour mortality (ß1=-0.668, 95% highest posterior density interval: -1.7 to 0.48). This posterior distribution indicates it is 8.1 times more likely that CSP transfusion improves 24-hour mortality than not. Sensitivity analyses across a spectrum of priors consistently produced posterior probabilities >81%. The beta-binomial model demonstrated a similar 86.2% probability that CSP transfusion reduced 24-hour mortality. These findings suggest a high likelihood of mortality benefit with early CSP transfusion in injured patients at risk of hemorrhagic shock and illustrate the added interpretive value of Bayesian analysis in trauma trials with low event rates. Level II-therapeutic/care management.

Sleep complaints are common in India, where recent meta-analytic estimates place the prevalence of insomnia among the highest reported anywhere. Over the same period, digital screen use has risen steeply, with very high daily smartphone use. Light-emitting diode (LED) screens are rich in short-wavelength ("blue") light. That part of the spectrum drives the intrinsically photosensitive retinal ganglion cells (ipRGCs) that set the circadian clock. Evening screen use can therefore blunt melatonin and push circadian timing later. Screen use is not, however, the same as the melanopic light dose actually reaching the retina. Associations between screen time and poor sleep may also reflect a later bedtime, mental and emotional arousal, notifications, and the type of content viewed. A lens would not change any of these. In this narrative review, we trace the melanopsin-ipRGC-suprachiasmatic nucleus pathway, ask how closely LED emission overlaps circadian photoreception, and weigh the evidence for spectacle-lens filtration as an adjunct to sleep hygiene, with a specific eye on India. Standard blue-light-filtering (BLF) lenses and longer-wavelength ("amber"/"orange") wavelength-selective lenses are held to the same evidentiary standard throughout. Systematic-review evidence rates the case that BLF lenses improve sleep as of low certainty, with findings that are indeterminate and heterogeneous rather than clearly negative. Trials of longer-wavelength lenses are small, clinically mixed, mostly unblinded, and at high risk of bias. Two pooled analyses of this literature reach different conclusions: an earlier one reported a small favorable effect on total sleep time, whereas a later analysis restricted to actigraphic outcomes from randomized crossover trials found no significant effect, with confidence intervals wide enough to indicate imprecision rather than a demonstrated absence of effect. What matters, recent work suggests, is a lens's measured melanopic filtering density rather than the color on its label, and this varies widely between products. Taken together, the evidence does not yet support recommending any spectacle-lens class as a treatment for disturbed sleep; the mechanistic case for lowering evening melanopic light is firmer than the clinical case for any particular lens. We set out why India is a priority setting and what an adequately powered, India-based trial would need to look like. Where filtration is used at all, it should sit alongside, not replace, established behavioral sleep hygiene and proper medical assessment.

Optical nanofibers provide a versatile platform for exploring strong light-matter interactions at the single-quantum level, a central goal of quantum optics. Their subwavelength diameter supports tightly confined guided modes with strong evanescent fields, enabling efficient coupling between photons and nearby atoms. By incorporating fiber Bragg gratings, nanofibers can form fully fiber-integrated high-finesse cavities, combining strong atom-photon coupling with efficient and low-loss optical input-output interfacing in the setting of cavity quantum electrodynamics (QED). In parallel, nanofiber systems naturally realize waveguide QED, where atoms interact strongly with propagating photons in a one-dimensional geometry. In this review, we introduce the underlying physical principles, summarize key experimental techniques and representative phenomena, and discuss prospects for applications in quantum information processing, quantum networks, and related quantum technologies.

Resistance to chemotherapy and tyrosine kinase inhibitor (TKI)-based therapy is the main reason for treatment failure in non-small cell lung cancer (NSCLC). Therefore, there is an urgent need to develop novel strategies to combat resistance. In this study, we designed and developed a novel, multi-targeted microRNA (miRNA) approach to overcome resistance to EGFR inhibitors. Specifically, the guide strand of the tumor suppressor miR-129 was modified by replacing cytidine with the nucleoside analog gemcitabine (Gem). The therapeutic potential of Gem-miR-129 was investigated in both in vitro and in vivo NSCLC model systems. Our results demonstrate that Gem-miR-129 is a potent inhibitor, with an IC50 in the low nanomolar range in NSCLC cell lines. Gem-miR-129 retains same nanomolar activity in both erlotinib- and osimertinib-resistant NSCLC cell lines. This potency is achieved through the dual mechanisms of the multi-targeted tumor suppressor miR-129, which suppresses HMGB1, YAP1, and PBX3, in conjunction with the expected therapeutic contribution of Gem following degradation of Gem-miR-129. A unique feature of Gem-miR-129 is its vehicle-free uptake in cultured NSCLC cells. Gem-miR-129 effectively inhibits NSCLC growth in a mouse model and significantly prolongs survival without overt toxicity under the tested conditions. Overall, Gem-miR-129 provides proof-of-concept for a novel tumor-suppressor miRNA-based therapeutic strategy for NSCLC and for overcoming TKI resistance.

Fluorescent voltage indicators are widely used to report relative changes in membrane potential, but mapping absolute voltages remains difficult. Here we present Voltage Measurement by Activated Photocycles (VMAP), a simple method for absolute voltage imaging based on a photophysical switch between voltage-insensitive and sensitive indicator states. VMAP requires no specialized hardware or additional labeling, and is applicable across species, sample preparations, and microscope configurations. Using VMAP, we quantified drug-induced shifts in neuronal resting potential, revealed the emergence of bioelectric patterns during multi-day recordings of human iPSC populations, and created 3D membrane-potential maps across whole live zebrafish embryos. By making absolute voltage imaging accessible from cellular to organismal scales and from milliseconds to days, VMAP opens a route to mapping bioelectrical organization in complex living systems.

The decision by the co-Editor-in-Chief of Regulatory Toxicology and Pharmacology, Prof. Martin van den Berg, to retract the 2000 review article by Williams, Kroes, and Munro has elicited widespread criticism within the scientific community. Issued in late 2025, the retraction decision cites procedural concerns including potential ghostwriting, undisclosed conflicts of interest, and omission of certain unpublished studies, invoking Committee on Publication Ethics guidelines despite lacking evidence of fraud or scientific flaws. This editorial argues that the retraction decision involves editorial overreach and misapplication of the guidelines. The alleged omissions stemmed from proprietary data access limitations that were disclosed in the original paper. Subsequent reviews by several independent expert panels and regulatory authorities with access to all glyphosate data, including the studies cited by the retracting editor, reached similar conclusions. Claims of ghostwriting were previously investigated and found lacking, including a declaration by EFSA as to the clarity of the conflict disclosures. The retraction's timing, reliance on litigation documents, and apparent biases that were not disclosed in the retraction notice raise questions of ideological interference. Absent substantive rebuttals based on scientific merit rather than speculative claims of inappropriate authorship and data access, this retraction decision sets a dangerous precedent for retroactive censorship, potentially chilling beneficial industry-academic collaborations and eroding trust in the integrity of scientific publishing. With the strongest conviction, we assert that retracting a paper without scientific flaws isn't protection-it is censorship. We therefore call for the immediate reversal of this flawed and unjustified retraction to preserve trust in peer-reviewed literature.

In recent years, activation of the immune system has been recognized as a key mechanism in supporting the therapeutic outcome of oncolytic virotherapy for cancer. Most studies have focused on T cells in the characterization of immune responses to therapy; however, the role of dendritic cells (DCs) in priming these cytotoxic T cell responses has been far less explored. rVSV-NDV is a chimeric oncolytic virus that causes a highly immunogenic cell death in infected tumor cells. In tumor-bearing mice, this leads to increased levels of circulating and tumor-infiltrating tumor-specific CD8+ T cells upon rVSV-NDV treatment. Here, we show that the rVSV-NDV-mediated immunogenic cell death leads to the activation of the dendritic cell subtypes, cDC1 and cDC2, in vitro and in vivo. Using wild-type (WT) and cDC1-deficient (BATF3KO) mice implanted with B16 melanoma lesions, we observed that the increase in circulatory, tumor-specific CD8+ T cells and the survival benefit conferred by rVSV-NDV tumor therapy depends on a functional cDC1 population. Finally, we demonstrate that rVSV-NDV therapy can be significantly augmented by the combined treatment with adoptively transferred cDC1 cells that were ex vivo activated and antigen-loaded by co-culture with rVSV-NDV-infected tumor cells.

Cyclin E1 (CCNE1), a critical regulator of cell cycle progression, has been implicated in various cancers; however, its prognostic significance and functional role across breast cancer (BC) subtypes remain inadequately defined. This study aims to comprehensively analyze CCNE1 mRNA expression and evaluate its potential as both a prognostic biomarker and a therapeutic guide. We analyzed CCNE1 mRNA expression using large-scale BC cohorts (TCGA, METABRIC, GEO) and assessed associations with tumour grade, overall survival, and mutation status. The muTarget platform was employed to investigate associations between CCNE1 expression and key genetic alterations. Furthermore, gene set enrichment analysis was performed to identify enriched biological pathways, and functional studies were conducted using mTORC1 inhibition in TP53-mutant, RB1-deficient TNBC cells to evaluate cell viability and CCNE1 expression levels. CCNE1 expression was significantly associated with higher tumour grade, overall survival, and distinct mutation statuses. Gene set enrichment analysis revealed enrichment of proliferation-related pathways, including G2-M checkpoint, E2F targets, and mTORC1 signaling in CCNE1-high tumors. Moreover, functional studies showed that mTORC1 inhibition successfully reduced CCNE1 expression and impaired viability in TP53-mutant, RB1-deficient TNBC cells. CCNE1 overexpression characterises a clinically aggressive subset of breast cancers, particularly TNBC. Targeting mTORC1 may represent a promising therapeutic approach in CCNE1-high, TP53-mutated, and RB1-deficient tumours, supporting the clinical utility of CCNE1 in patient stratification and targeted therapy.

Noninvasive tests are well validated in metabolic dysfunction-associated steatotic liver disease, but evidence in metabolic dysfunction and alcohol-associated liver disease (MetALD) and alcohol-associated liver disease (ALD) is limited. We evaluated noninvasive test-based clinical care pathways for fibrosis risk stratification in MetALD and ALD. This is a multinational, multicenter, cross-sectional study across 35 centers in 16 countries (2013-2025), including adults with MetALD or ALD. Fibrosis was assessed by liver biopsy and/or vibration-controlled transient elastography (VCTE). In biopsy-proven participants, we analyzed the sequential pathway (Fibrosis-4 [FIB-4] first, followed by VCTE for indeterminate FIB-4) to identify advanced fibrosis (≥F3). Diagnostic accuracy was assessed using the AUC. Among 893 participants (41.3% MetALD and 58.7% ALD), the median age was 52 [43.0-61.0] years, and 79.4% were male. The estimated prevalence of advanced fibrosis was 45% (32.2% in MetALD and 54.0% in ALD). Participants with MetALD had a more dysmetabolic profile but lower fibrosis stages than ALD. Among biopsy-proven participants, FIB-4 AUC was 0.720, and VCTE AUC was 0.833. FIB-4 performed better in MetALD than ALD (AUC 0.773 vs. 0.540), while VCTE accuracy was similar across groups. In the sequential pathways, the false-negative rate for advanced fibrosis (misclassified as low risk) was 6.8% (4.9% MetALD and 11.3% ALD). In biopsy-proven patients, FIB-4 performance was acceptable in MetALD but substantially weaker in ALD. The standard 2-step pathway performed adequately in MetALD but missed a clinically meaningful proportion of advanced fibrosis in ALD.

Variants in the glucocerebrosidase gene (GBA1) are the predominant genetic risk factor for Parkinson's disease (PD), often accelerating disease progression. While biological sex modulates PD progression, the longitudinal association between rasagiline (a monoamine oxidase-B [MAO-B] inhibitor) and motor outcomes in GBA1-associated Parkinson's disease (GBA1-PD) remains unclear. This retrospective cohort study (2019-2026) analyzed 259 patients with PD (106 females, 153 males) with a median follow-up of 1.56 years to evaluate the association between rasagiline use and motor decline, emphasizing sex-stratified outcomes. Motor progression was evaluated using the Movement Disorder Society-Unified Parkinson's Disease Rating Scale part III (MDS-UPDRS-III). Rates of change were calculated using sex-stratified Generalized Estimating Equations models, with adjustment for age at diagnosis to evaluate treatment effects and sex-specific associations. Among 259 patients, rasagiline use was associated with a significantly slower annual rate of motor decline (Slope Difference: -0.95; p = 0.03). In the GBA1-PD subgroup, females using rasagiline exhibited a clinically relevant slower rate of progression (approximately 1 point/year on the MDS-UPDRS-III) compared with non-users, although not statistically significant (p = 0.08); no association was observed in males. These findings suggest a potential sex-specific association of rasagiline with motor progression in GBA1-PD. Results highlight the importance of sex-stratified analyses to support personalized therapeutic approaches for PD genetic variants.

Glycogen is a highly conserved macromolecule across species, and its visualization provides critical insights into both physiological processes and disease states. Existing approaches for glycogen imaging in Caenorhabditis elegans rely primarily on traditional microscopy slides, which introduce variability in image acquisition and downstream data analysis, limit throughput, and require substantial hands-on time and technical expertise. Here, we present a standardized, cost-effective, and high-throughput imaging method that enables efficient visualization and quantification of glycogen in C. elegans. Our approach utilizes a custom-designed three-dimensional pad containing two to four chambers, allowing control and experimental samples to be processed simultaneously under identical conditions. Worms are exposed to iodine crystals, ensuring uniform staining while minimizing reagent use and handling variability. Imaging is performed using a simple binocular microscope, and analysis is conducted in Fiji, making the workflow accessible to laboratories with minimal specialized equipment or training. This method also reduces technical variability, shortens turnaround time, and requires only basic reagents and expertise, making it well-suited for both research and teaching laboratories. Importantly, the platform is readily adaptable to other nematode species and scalable for large-scale genetic or pharmacological screening applications. Together, this workflow minimizes technical variability and provides a robust platform for comparative glycogen analysis in C. elegans. Key features • Standardized glycogen staining method allows less data variability. • Provides a quantitative tool to measure glycogen buildup in C. elegans. • Requires a customized pad for imaging. • Macro is available for batch processing.