In the continually evolving field of anesthesiology, recent research spearheaded by Liu, Shi, Hu, and colleagues has unveiled compelling evidence that challenges and potentially reshapes traditional approaches to anesthesia in older adults undergoing surgery for hip fractures. Their retrospective study, published in BMC Geriatrics in 2026, meticulously examines the efficacy and safety profile of unilateral epidural anesthesia specifically tailored for geriatric patients with hip fractures—a demographic notoriously susceptible to complications during and after surgery.

Hip fractures in the elderly represent a significant clinical challenge worldwide, characterized by high morbidity and mortality rates. Managing pain effectively while minimizing systemic side effects from anesthesia remains a crucial concern for anesthesiologists and surgeons alike. Traditional modalities often involve bilateral epidural or general anesthesia; however, these methods can carry notable risks, including hemodynamic instability and prolonged motor blockade. This study shifts the spotlight onto unilateral epidural anesthesia, a targeted anesthetic technique designed to provide localized nerve blockade on the operative side only.

Unilateral epidural anesthesia distinguishes itself by confining the anesthetic effect predominantly to the surgical side, thereby reducing sympathetic nervous system disruption contralaterally. This precision results in better hemodynamic stability, which is particularly advantageous in older patients frequently burdened by cardiovascular comorbidities. The retrospective analysis conducted by Liu et al. rigorously evaluates patient outcomes, highlighting that unilateral epidural anesthesia may significantly diminish perioperative complications without sacrificing analgesic efficacy.

The study’s methodology encompasses a comprehensive evaluation of clinical records, encompassing various parameters including hemodynamic changes, pain scores, motor function recovery, and incidences of postoperative delirium—a common and serious complication in the elderly. Quantitative data reveal that patients receiving unilateral epidural anesthesia experienced a more stable intraoperative blood pressure profile and reduced incidence of postoperative cognitive dysfunction, underscoring the approach’s beneficial role beyond pain control alone.

Technically, the procedure involves the careful placement of an epidural catheter at thoracolumbar levels corresponding to the surgical site, followed by administration of low-concentration local anesthetics. This approach fosters segmental blockade, sparing contralateral nerve roots and thereby encouraging earlier mobilization and reduced nursing care needs post-surgery. The pharmacodynamics of this anesthetic technique emphasize minimizing systemic absorption and maximizing localized action, which collectively contribute to the observed safety profile.

Another compelling aspect underscored in the research is the opioid-sparing effect of unilateral epidural anesthesia. Opioid analgesics, although effective, carry risks of respiratory depression, constipation, and delirium—ailments especially precarious for the elderly. By reducing opioid requirements, unilateral epidural anesthesia could potentially curtail these adverse effects, enhancing postoperative recovery trajectories and overall patient satisfaction.

Moreover, Liu and colleagues discuss the implications of unilateral epidural anesthesia on resource utilization within healthcare settings. The technique’s association with fewer hemodynamic disturbances reduces the need for advanced cardiovascular monitoring intraoperatively and in the intensive care environment. This efficiency gain could translate into shorter hospital stays and decreased healthcare expenditure, a critical consideration in systems strained by aging populations.

The retrospective nature of the study, while inherently limiting causal inferences, nonetheless offers a robust foundation for future prospective randomized trials. Such investigations could further illuminate the mechanistic underpinnings responsible for the favorable outcomes observed and refine patient selection criteria to optimize individualized anesthesia care in orthogeriatrics.

Technical challenges associated with unilateral epidural anesthesia are not overlooked. Precise catheter placement requires skilled practitioners well-versed in fluoroscopic or ultrasound-guided techniques to ensure unilateral spread and minimize inadvertent bilateral blockade. The study underscores the necessity for comprehensive training and corroborative imaging to maximize the procedure’s efficacy and safety.

From a physiological standpoint, the selective sympathetic blockade innate to unilateral epidural anesthesia not only stabilizes hemodynamics but also mitigates neuroinflammatory cascades triggered by surgical trauma. Emerging evidence suggests that blunting this inflammatory response could reduce the risk of postoperative cognitive decline, an area ripe for further interdisciplinary research bridging anesthesia, neurology, and geriatrics.

Complementary to these clinical insights, the study also revisits pharmacological considerations. The choice of local anesthetics, concentration gradients, and adjuvants such as clonidine or dexmedetomidine are deliberated, emphasizing the balance between achieving adequate sensory blockade and preserving motor function. This pharmacological fine-tuning is pivotal for enabling early postoperative mobilization—a key determinant of successful rehabilitation in elderly hip fracture patients.

Patient-centric outcomes encapsulated in the study extend beyond clinical parameters to patient-reported pain and satisfaction scores. The positive feedback corroborates that unilateral epidural anesthesia not only suits physiological and logistical needs but also aligns with patient comfort and quality of life goals, reinforcing its clinical appeal.

Given the growing incidence of hip fractures globally, driven principally by demographic shifts toward older age groups, the implications of this study are profound. It advocates for a paradigm shift in orthopedic anesthesia, promoting a minimally disruptive approach aligned with geriatric physiology and tailored to reduce perioperative risk, thus potentially setting a new standard of care.

The findings of Liu et al. resonate particularly in the context of value-based healthcare, where interventions delivering superior outcomes with cost-effectiveness are paramount. The integration of unilateral epidural anesthesia into clinical pathways could redefine perioperative protocols for vulnerable populations, fostering enhanced recovery and reduced healthcare burden.

In conclusion, this pivotal retrospective study paves the way for enhanced anesthetic strategies that prioritize safety without compromising efficacy. The promise of unilateral epidural anesthesia for older adults with hip fractures represents not just an incremental advance but a stride toward precision medicine in anesthesiology. Continued research and clinical adoption stand poised to transform surgical care paradigms, ultimately improving the lives of millions of elderly patients worldwide.

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Subject of Research: The application and outcomes of unilateral epidural anesthesia in elderly patients undergoing hip fracture surgery.

Article Title: A retrospective study on the application of unilateral epidural anesthesia in older patients with hip fracture.

Article References:
Liu, P., Shi, X., Hu, J. et al. A retrospective study on the application of unilateral epidural anesthesia in older patients with hip fracture. BMC Geriatr (2026). https://doi.org/10.1186/s12877-026-07859-z

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Atherosclerosis remains the foremost cause of cardiovascular disease-related morbidity and mortality globally, posing a substantial challenge to healthcare systems. Although traditional risk factors such as diet, lifestyle, and genetics have been extensively studied, recent advances have illuminated the pivotal role played by epigenetic mechanisms in shaping the onset and progression of atherosclerotic disease. Epigenetics, the reversible modulation of gene expression without alterations to the DNA sequence, encompasses DNA methylation, histone modifications, and non-coding RNAs, all of which intricately orchestrate cellular behavior within vascular tissues.

Emerging research reveals that DNA methylation patterns, both globally across the genome and in gene-specific loci, critically regulate cellular proliferation and inflammatory responses integral to atherogenesis. Hypomethylation or hypermethylation at particular sites can drastically affect the transcriptional activity of genes responsible for maintaining vascular homeostasis. This phenomenon underscores a dynamic regulatory system where environmental cues and pathological stimuli can induce lasting epigenomic changes that propagate vascular dysfunction and inflammation.

Histone post-translational modifications add another sophisticated layer to this epigenetic landscape. Primarily involving acetylation and methylation of histone proteins, these modifications influence chromatin structure and, consequently, gene accessibility. Within atherosclerotic plaques, histone modifications have been shown to govern networks of genes related to lipid metabolism, cellular plasticity, and inflammatory signaling. Such modifications enable vascular cells to adapt to inflammatory and metabolic stress by modulating transcriptional programs essential for plaque development and instability.

Non-coding RNAs have further expanded the complexity of epigenetic regulation within the vascular milieu. Long non-coding RNAs (lncRNAs) shape the transcriptomic profiles of specific cell types and exert control over the localization and activity of epigenetic enzymes. This targeting ensures that epigenetic remodeling is not only precise but also tailored to cellular needs in the context of vascular remodeling. Concurrently, microRNAs (miRNAs), small regulatory RNAs, predominantly mediate post-transcriptional gene silencing but have been identified to participate in non-canonical functions that influence vascular cell phenotype and immune responses.

The integration of multi-omics approaches, combining epigenomics, transcriptomics, and proteomics, has revolutionized our understanding of the cell-specific epigenetic contributions in atherosclerosis. These technological advancements enable the dissection of complex intercellular interactions within plaques and facilitate the mapping of genetically associated loci to discrete epigenetic modifications. This multidimensional insight is vital to unraveling the heterogeneity of atherosclerotic lesions and their diverse clinical manifestations.

In vascular endothelial cells, epigenetic alterations modulate barrier function, inflammation, and response to shear stress, all of which are critical in the initial stages of atherogenesis. Endothelial dysfunction triggered by epigenetic dysregulation sets the stage for immune cell recruitment and plaque formation. Meanwhile, vascular smooth muscle cells (VSMCs) exhibit remarkable plasticity through epigenetic reprogramming that drives their phenotypic switch from a contractile to a synthetic state, facilitating extracellular matrix remodeling and plaque stability or vulnerability.

Immune cells within the atherosclerotic microenvironment are also subject to profound epigenetic modulation. Macrophages, T cells, and other leukocytes display distinct epigenetic signatures that influence their activation states and inflammatory profiles. Epigenetic memory within these immune populations can perpetuate chronic vascular inflammation, underscoring the need for targeted interventions that modulate immune cell epigenomes to mitigate atherosclerotic progression.

Preclinical studies have leveraged these mechanistic insights to explore epigenetic drug candidates capable of attenuating plaque burden and vascular inflammation. Histone deacetylase inhibitors, DNA methylation modulators, and RNA-based therapeutics have demonstrated efficacy in experimental models, highlighting their potential to recalibrate aberrant gene expression patterns driving disease. However, challenges remain in achieving cell-type specificity, minimizing off-target effects, and ensuring the durability and safety of such interventions in humans.

A critical hurdle for translational success lies in the delivery mechanisms for epigenetic therapies. Nanoparticle-based systems and ligand-targeted delivery platforms are under investigation to enhance precision targeting of vascular and immune cells within plaques. These delivery technologies aim to maximize therapeutic benefit while circumventing systemic toxicity, thereby advancing the clinical applicability of epigenetic modulators.

Long-term safety is another paramount consideration as epigenetic drugs inherently affect gene regulation, potentially leading to unforeseen consequences. Rigorous preclinical evaluation and carefully designed clinical trials are imperative to balance efficacy with safety, ensuring that epigenetic therapies can be integrated into cardiovascular medicine without triggering deleterious off-target effects.

The prospect of leveraging epigenetic regulation heralds a transformative shift in cardiovascular therapeutics, enabling precision medicine tailored to an individual’s unique epigenomic landscape. By elucidating the dynamic and reversible nature of epigenetic modifications in vascular cells and immune populations, researchers are charting new pathways to mitigate atherosclerosis beyond conventional lipid-lowering and anti-inflammatory strategies.

Continued exploration into the interplay between genetic predisposition and environmental influences mediated by epigenetic mechanisms promises to deepen our understanding of atherosclerosis pathobiology. This holistic view integrates molecular, cellular, and systemic insights, empowering the development of sophisticated therapeutics capable of interrupting the disease process at its regulatory roots.

In summary, the frontier of atherosclerosis research lies at the intersection of epigenetics and vascular biology. The potential to manipulate gene expression programs with high specificity and reversibility offers an unprecedented opportunity to combat the global burden of cardiovascular disease. As the field advances, collaboration across disciplines and innovative technological approaches will be essential to realize the therapeutic promise of epigenetic modulation in clinical practice.

With ongoing efforts focused on unraveling cell-specific epigenetic mechanisms, refining drug delivery technologies, and ensuring long-term treatment safety, the era of epigenetics-driven precision cardiology is on the horizon. This paradigm shift not only holds the key to diminishing the impact of atherosclerosis but also exemplifies the broader potential of epigenetic therapies across complex diseases.

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Subject of Research: Epigenetic regulation mechanisms in atherosclerosis and their potential for therapeutic intervention.

Article Title: Epigenetic regulation in atherosclerosis and its therapeutic potential

Article References:
Santovito, D., Atzler, D. & Weber, C. Epigenetic regulation in atherosclerosis and its therapeutic potential. Nat Rev Cardiol (2026). https://doi.org/10.1038/s41569-026-01313-8

Image Credits: AI Generated

Scientists found that some inherited traits can bypass the traditional rules of genetics, revealing a surprising new layer of inheritance beyond DNA. For more than a century, Gregor Mendel’s laws of inheritance have served as the foundation of genetics. But new research suggests that inheritance can be more complicated than the DNA sequences passed from [...]

Most people think of gum disease as a problem caused mainly by poor brushing or not visiting the dentist often enough. While plaque and harmful bacteria are important causes, scientists are increasingly learning that diet, inflammation, stress, and general health also influence the condition. A new study from King’s College London has added another piece […]

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Treating high blood pressure seems simple in theory. Doctors diagnose the condition, prescribe medicines, and expect blood pressure to improve. In reality, controlling hypertension is often much more complicated. High blood pressure is frequently called a silent killer because it can quietly damage the body for years without causing noticeable symptoms. The condition greatly increases […]

The post Could a Urine Test Reveal Why High Blood Pressure Treatments Sometimes Fail? appeared first on Knowridge Science Report.

For many years, e-cigarettes and vapes have been promoted as a safer alternative to traditional cigarettes. Because they do not burn tobacco, many people assumed they were far less harmful than smoking. Their fruity flavors, modern designs, and marketing campaigns reinforced the idea that vaping was a cleaner and healthier choice. Some health experts even […]

The post Huge Study Links E-Cigarettes to Higher Lung Cancer Risk appeared first on Knowridge Science Report.

Type 2 diabetes is becoming one of the biggest health challenges around the world. Millions of people are living with the disease, and many more are at risk of developing it. Type 2 diabetes happens when the body can no longer use insulin properly, causing blood sugar levels to rise. Over time, high blood sugar […]

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Traumatic brain injury, often called TBI, happens when a blow, bump, or sudden jolt to the head damages the brain. These injuries can range from mild concussions to severe brain damage that changes a person’s life forever. Every year, millions of people around the world experience traumatic brain injuries. Older adults are especially vulnerable because […]

The post Brain Disorders and Head Injuries May Be More Closely Connected Than We Thought appeared first on Knowridge Science Report.

Most people rarely think about their sense of smell or taste. The smell of fresh coffee, the taste of a favorite family recipe, or the scent of flowers are such ordinary experiences that they often go unnoticed. It is only when these senses disappear that many people realize how important they are. A new study […]

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In a groundbreaking study published in Nature, researchers have illuminated the subtle yet profound effects of confined cellular migration on the genomic integrity of developing neurons. This investigation, spearheaded by Zhang et al., delves into the enigmatic landscape of DNA double-strand breaks (DSBs) triggered by migration through physically restrictive environments—an event that is essential during brain development. The study reveals that such DNA damage, although non-lethal, accumulates in specific chromatin regions and leads to long-lasting transcriptional changes, shedding new light on neural physiology and potentially neurodegenerative processes.

The team utilized END-seq, a sophisticated genome-wide technique designed to detect double-strand breaks with base-pair precision. They focused on cerebellar granule neurons (CGNs), which were forced to migrate through micro-pores measuring either 3 micrometers or 8 micrometers. This experimental setup mimics the physical confinement neurons experience during their natural migration in the developing brain. Surprisingly, the analysis showed no enrichment of DSBs at well-known genetic hotspots or regulatory motifs, suggesting a non-random but unconventional pattern of DNA breakage.

Further classification of the DSBs unveiled a striking preference for heterochromatic regions, particularly lamina-associated domains (LADs), which are generally repressive chromatin zones linked to the nuclear periphery. The clusters of DSBs were notably depleted from active promoters and enhancers, indicating that the migratory stress preferentially compromises regions of genomic inactivity or tightly packed chromatin. Intriguingly, the damage was also significantly enriched in repetitive DNA elements, especially long interspersed nuclear elements (LINEs), hinting at a possible vulnerability of retrotransposons under mechanical strain.

The authors also analyzed chromatin loop anchor sites, which typically harbor proteins such as CTCF and cohesin subunit RAD21, but found no significant alteration in DSB accumulation within these sites. Additionally, they examined transcription start sites and gene bodies without detecting marked shifts in DNA damage correlating with transcriptional activity or gene length, including those of notably long genes linked to neuronal connectivity. This evidence points towards a topological and functional disconnect between confined migration-induced DNA breaks and classical topoisomerase II beta (TOP2β) hotspots involved in gene regulation.

Experimentally, the research extended beyond in vitro models; the team studied cerebellar cortex tissues from genetically modified mice deficient in DNA Ligase IV (LIG4), a key enzyme in non-homologous end joining (NHEJ), a primary DNA repair pathway. These mice exhibited accumulation of unrepaired DSBs, which, akin to their in vitro counterparts, showed no consistent site-specificity but were enriched in similar inert chromatin domains and repetitive sequences. The lack of damage enrichment in actively transcribed regions contrasted with the typical topological DNA breaks observed in genome regulation, affirming the unique nature of migration-induced genomic insults.

To explore the long-term consequences of these persistent DSBs, the researchers performed bulk RNA sequencing on cerebellar tissue from control and LIG4-deficient mice at two months of age. The analysis uncovered 336 genes significantly differentially expressed. Notably, genes involved in neuronal differentiation and synaptic function were downregulated, whereas genes associated with stress and immune responses, particularly those expressed by microglia and immune cells, were upregulated. These transcriptional alterations suggest that incomplete DSB repair following migration influences neuronal function and potentially primes an inflammatory-like gene expression environment.

Further validation through immunofluorescence staining confirmed the decreased expression of MYO15A—a gene critical to neuronal physiology—in the granule neurons of mutant mice. Concurrently, CD86, a marker of immune activation, was elevated in cerebellar microglia. However, contrary to expectations, classical hallmarks of microglial activation and neuroinflammation were absent, hinting at a nuanced immune response possibly distinct from pathological states. Moreover, the gene expression profile differed markedly from normal ageing patterns in the cerebellum, underscoring a unique molecular signature tied to DNA damage rather than degeneration or senescence.

Intriguingly, a notable overlap was detected between the gene clusters upregulated in LIG4-deficient mice and those observed in cortical neurons exhibiting γH2AX foci—a marker of DNA damage—in early neurodegeneration models. This parallel points to a mechanistic link between migration-induced DNA damage and neurodegenerative processes, positing confined migration as a previously underappreciated source of genomic stress that might influence disease susceptibility later in life.

The findings challenge traditional notions that DNA damage in neurons is predominantly tied to transcriptional mechanics or enzymatic activity at gene regulatory elements. Instead, the physical constraints of cellular migration emerge as a novel driver of genome instability, especially within transcriptionally silent and structurally repressive chromatin. These insights compound our understanding of neurodevelopmental biology and illuminate how mechanical forces can precipitate subtle genomic alterations with lasting transcriptional consequences.

Methodologically, the integration of END-seq with chromatin accessibility assays like ATAC-seq, histone modification ChIP-seq, and RNA sequencing provided a multidimensional approach to dissecting the genome-wide effects of confined migration. This comprehensive epigenomic profiling enabled the precise localization of DSBs and their contextual annotation within chromatin states, revealing the vulnerability of specific nuclear compartments to migratory stress.

By linking persistent DNA lesions to transcriptional rewiring, the study suggests a model in which unresolved damage in perinuclear heterochromatin may disrupt chromatin organization or nuclear architecture, ultimately modulating gene expression networks critical for neuronal maturation and function. The absence of typical DNA damage markers at regulatory elements also highlights that different mechanisms underpin the observed breaks, possibly related to mechanical strain or physical deformation during migration rather than enzymatic topological activity.

The clinical and biological implications of these findings are profound. They provoke questions about how developmental neuronal migration, a fundamental process shaping brain circuitry, might inadvertently introduce genomic perturbations that contribute to neurodevelopmental disorders or sensitize neurons to later insults. Additionally, they raise the prospect that interventions aimed at enhancing DNA repair capacity or modulating nuclear mechanics could mitigate such damage, offering new therapeutic avenues for neuroprotection.

Ultimately, this study redefines our understanding of the interplay between physical cellular processes and genome stability in the nervous system. It underscores the importance of considering mechanical forces as integral contributors to genomic integrity and neuronal health, bridging gaps between developmental biology, genomics, and neurodegeneration research. As research advances, these revelations pave the way for novel strategies to preserve neuronal function amidst the inherent challenges of brain development.

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Subject of Research: Genomic integrity and DNA damage induced by confined migration in developing neurons.

Article Title: Confined migration induces non-lethal DNA damage in developing neurons.

Article References:
Zhang, Z., Canela, A., Kurisu, J. et al. Confined migration induces non-lethal DNA damage in developing neurons. Nature (2026). https://doi.org/10.1038/s41586-026-10648-8

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41586-026-10648-8

Many people think menopause mainly causes symptoms such as hot flashes and mood swings. However, one of the biggest health changes during menopause happens silently inside the body. Bones begin to lose strength. Healthy bones may look solid, but they are constantly changing. Throughout life, old bone is removed and new bone is created. This […]

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In a groundbreaking advancement that could revolutionize cancer prognosis and treatment, a team of researchers led by Liu, X., Dai, F., and Dai, J., has unveiled a sophisticated multimodal multitask deep learning system for grading management in non-small cell lung cancer (NSCLC). Published recently in Nature Communications, this innovative approach integrates diverse data modalities through an advanced artificial intelligence framework, demonstrating unprecedented accuracy and efficiency in tumor grading and patient stratification—key factors in tailoring personalized therapies and improving patient outcomes.

Non-small cell lung cancer remains one of the leading causes of cancer-related mortality worldwide, largely due to its heterogeneity and the challenge of precise tumor grading. Traditional grading methods rely heavily on histopathological analysis, which, while indispensable, faces limitations in capturing the complex biological and morphological variations across patients. This novel multimodal multitask network leverages deep learning’s capacity to extract nuanced features across multiple data types, including histology images, radiographic scans, and molecular profiles, effectively capturing the multidimensional nature of the disease.

The core innovation of this system lies in its multitask learning architecture, which simultaneously addresses multiple clinical endpoints—tumor grading, staging, and survival prediction—within a unified model. This approach contrasts with previous single-task models that focus on one predictive target, often neglecting the interdependencies among clinically significant tasks. By jointly optimizing these objectives, the model enhances its robustness and clinical utility, improving prognostic accuracy and enabling more informed decision-making.

From a technical perspective, the deep learning model employs convolutional neural networks (CNNs) tailored to each data modality. For imaging data, sophisticated CNN architectures with residual connections enable hierarchical feature extraction, while genomic and proteomic data are processed via fully connected layers, integrated through fusion mechanisms within the network. Crucially, the system employs attention mechanisms that dynamically weigh contributions from each data source, ensuring that the most relevant features guide the tumor grading process. This multimodal fusion enhances interpretability, as clinicians can trace back which data aspects influence the model’s predictions.

The training dataset comprises an extensive cohort of NSCLC patients, encompassing thousands of digitized histopathology slides, CT images, and matched molecular data. The researchers implemented rigorous preprocessing pipelines to normalize and augment the data, addressing variability inherent in clinical datasets. Importantly, domain adaptation techniques were employed to mitigate batch effects and imaging protocol heterogeneity, ensuring the model’s generalizability across different clinical settings and patient populations.

Performance metrics reported in the study underscore the system’s superiority over conventional grading methods and previous AI models. With an area under the receiver operating characteristic curve (AUC-ROC) exceeding 0.90 for tumor grading tasks, the model exhibits remarkable sensitivity and specificity. Notably, survival prediction tasks achieved similarly high accuracy, enabling stratification of patients into risk categories with potential to guide treatment intensification or de-escalation.

In addition to diagnostic accuracy, the system’s design emphasizes clinical workflow integration. The researchers developed an interactive platform allowing pathologists and oncologists to visualize model outputs alongside raw data, fostering collaborative interpretation. This interface incorporates uncertainty quantification and confidence scores, aiding clinicians in evaluating prediction reliability and assimilating AI-driven insights with clinical judgment.

The researchers also addressed ethical and regulatory considerations critical for clinical deployment. Data privacy was preserved through federated learning techniques during model training, circumventing the need for centralized data storage and enabling multi-institutional collaboration without compromising patient confidentiality. Moreover, the model’s transparent architecture and interpretability features facilitate compliance with emerging AI governance frameworks and regulatory approvals.

Beyond the immediate clinical implications, this study exemplifies the transformative potential of deep learning for precision medicine. By capturing tumor heterogeneity through multimodal data fusion, it paves the way for dynamic tumor characterization that adapts to evolving cancer biology over time, potentially informing adaptive therapy paradigms. Furthermore, the model’s multitask structure could be extended to other malignancies or complex diseases characterized by multifactorial phenotypes.

The authors highlight several avenues for future research, including prospective clinical trials to assess real-world efficacy and impact on treatment outcomes. Plans to incorporate longitudinal patient data hold promise for modeling disease progression and therapy resistance. Additionally, incorporating emerging data modalities such as circulating tumor DNA and spatial transcriptomics could further refine the grading system’s sensitivity and specificity.

In summary, this landmark study ushers in a new era of AI-driven oncology, where deep learning models not only automate grading but also synthesize heterogeneous clinical data to empower personalized management in NSCLC. By bridging computational innovation and clinical applicability, it stands to significantly enhance diagnostic precision, treatment planning, and ultimately patient survival in a notoriously challenging cancer type.

As research continues to unravel the complexities of NSCLC, such sophisticated AI frameworks represent vital tools in the quest to deliver more effective, individualized care. The collaborative effort showcased by Liu, Dai, and colleagues sets a compelling precedent for harnessing multimodal data integration and multitask deep learning to tackle other pressing challenges in oncology and beyond.

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Subject of Research: Multimodal multitask deep learning for tumor grading and management in non-small cell lung cancer

Article Title: Multimodal multitask deep learning for grading management system in non-small cell lung cancer

Article References: Liu, X., Dai, F., Dai, J. et al. Multimodal multitask deep learning for grading management system in non-small cell lung cancer. Nat Commun (2026). https://doi.org/10.1038/s41467-026-74474-2

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A groundbreaking analysis of 173,303 exomes and genomes from the Pakistan Genome Resource (PGR) has unveiled compelling insights into the genetic architecture of human diseases and the therapeutic potential of loss-of-function (LoF) variants. This expansive dataset offers unprecedented resolution into homozygous loss-of-function (homLoF) mutations across diverse genes, providing critical human biological data that challenge and refine preclinical models. The ramifications for drug discovery are profound, underscoring the value of population-based genomic studies in elucidating gene function and safety profiles of potential therapeutics.

The PGR study corroborated previously established phenotypic associations for numerous homLoF variants. For instance, homozygous LoF mutations in LDLR were linked to hypercholesterolemia, while variants in LPL were associated with elevated triglyceride levels. Similarly, ANGPTL3 and APOB homLoF carriers exhibited notably reduced cholesterol and triglyceride profiles, whereas variants in ADCY3, POMC, MC4R, and MRAP2 were implicated in obesity phenotypes. These observations not only validate the penetrance of key metabolic genes but also affirm the rigorous phenotyping framework employed by the PGR.

Delving into therapeutically relevant homLoF variants, the study sheds light on the nuanced interplay between genotype and phenotype in neurodegeneration. LRRK2, a well-known protein kinase whose gain-of-function variants increase Parkinson’s disease risk, was examined in the context of loss-of-function. Notably, two PGR participants harboring homozygous LRRK2 pLoF variants exhibited early-stage kidney disease, a phenotype absent in heterozygous carriers. This human evidence mirrors renal dysfunction observed in LRRK2 knockout rodent models and preclinical trials with LRRK2 inhibitors in primates, suggesting a need for vigilant renal monitoring in therapeutic contexts targeting LRRK2.

In the realm of metabolic disease, a participant with a homLoF variant in SLC2A4—the gene encoding GLUT4—demonstrated type 2 diabetes, aligning with experimental models where GLUT4 deficiency impairs glucose homeostasis. Contrastingly, homLoF variants in DENND1B, previously linked to obesity and implicated in MC4R signaling pathways, did not confer obesity phenotypes in the cohort. This could indicate a lack of functional penetrance of DENND1B in human energy balance, differing substantially from prior murine models. Moreover, carriers of homLoF mutations in POMC, MC4R, and MRAP2 exhibited elevated BMI, reinforcing their contributory role to obesity.

Cardiovascular research insights emerged with RXFP1, a gene encoding a receptor extensively studied for its role in fertility, fibrosis, and cardiac function. Despite the gene’s pivotal role in murine reproductive and cardiovascular models—where its absence causes pronounced phenotypes—16 PGR individuals with RXFP1 homLoF variants spanned ages 30 to 73 years with no consistent deficits. Subtle associations with reduced waist-to-hip ratio and myocardial infarction risk were noted, and echocardiographic evaluations revealed mild variations in cardiac function among some homozygotes. Such findings suggest that the translational relevance of RXFP1 as a therapeutic target may be overestimated from rodent data, urging a recalibration of expectations for RXFP1 agonist therapies.

The hepatoprotective potential of CIDEB inhibition also gained support from PGR findings. Fourteen individuals homozygous for CIDEB loss-of-function variants displayed no liver disease, and burden analyses correlated CIDEB deficiency with decreased levels of liver enzymes ALT and AST and a reduced risk of non-alcoholic fatty liver disease. This human genetic evidence bolsters the rationale for targeting CIDEB therapeutically with siRNA or other modalities, highlighting an encouraging safety profile for chronic intervention.

Surprising evolutionary biology insights were uncovered in the reproductive gene PRDM9, a histone methyltransferase essential for meiotic recombination hotspot determination. While Prdm9 knockout mice exhibit infertility, PGR identified multiple human homLoF variant carriers of PRDM9 with proven fertility and successful reproduction. This stark species divergence reveals that PRDM9’s indispensability in meiosis is not conserved in humans, emphasizing the complexity of translating mouse genetic models to human biology.

Sensory gene analyses revealed functionally impactful homLoF mutations in TRPM8, an ion channel activated by cold stimuli. RBG cohort phenotyping demonstrated that carriers exhibited delayed cold-induced pain sensitivity and increased tolerance to cold-related discomfort, aligning with murine knockout models. Intriguingly, genome-wide association studies link TRPM8 variants to migraine susceptibility, positing TRPM8 inhibition as a promising therapeutic avenue. The PGR data indicate that complete loss of TRPM8 is generally well-tolerated, mitigating safety concerns for pharmacological antagonism targeting migraine prevention.

Collectively, these results highlight the critical importance of integrating large-scale human genomic data with functional assays to delineate gene-disease relationships and therapeutic potential. The PGR exemplifies how comprehensive population-based sequencing can validate, refine, or refute biological assumptions derived from animal models, fostering a more precise paradigm for drug target validation. By profiling rare homLoF variants and linking them with detailed phenotypic data, the study provides invaluable resources for developing safer, more effective genetic-driven therapies.

This study also accentuates the value of consanguineous populations, such as the Pakistani cohort, which enrich for homozygous rare variants and enable the detection of recessive phenotypes difficult to observe in outbred populations. Such datasets maximize the discovery power for identifying natural human knockouts, thereby informing on both the efficacy and potential deleterious effects of gene inactivation.

Beyond specific gene findings, the broader implication is a caution against uncritical extrapolation from model organisms to human physiology. While murine models remain indispensable, discrepancies evidenced in PRDM9 and RXFP1 underscore that human genetic data are indispensable for accurate target validation and safety assessment. This alignment between genotype, phenotype, and therapeutic action forms the cornerstone of precision medicine.

As the PGR and similar initiatives continue to expand, the integration of genomics with phenotypic and clinical data will catalyze a new era of therapeutic development truly grounded in human biology. The promise of harnessing human loss-of-function variants lies not only in uncovering disease mechanisms but also in guiding drug discovery toward targets with validated human safety and efficacy profiles, ultimately accelerating the path from bench to bedside.

This landmark study published in Nature offers a crucial template for leveraging population genomics in drug development, emphasizing the necessity of human genetic evidence to underpin the next generation of therapies. The insights gleaned provide a roadmap for more rational, genetics-informed clinical decision-making, heralding a future where personalized medicine and pharmacogenomics converge to transform healthcare.

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Subject of Research: Genomic analysis of homozygous loss-of-function variants in the Pakistan Genome Resource and their implications for human disease and drug target validation.

Article Title: Analysis of 173,303 exomes and genomes in the Pakistan Genome Resource.

Article References:
Koch, C., Khalid, S., Khan, M.Z. et al. Analysis of 173,303 exomes and genomes in the Pakistan Genome Resource. Nature (2026). https://doi.org/10.1038/s41586-026-10667-5

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41586-026-10667-5

In an unprecedented advancement for neurodegenerative disease research, a team led by Busquets, Li, Syed, and colleagues has unveiled iSCORE-PD, an innovative isogenic stem cell repository designed explicitly to accelerate Parkinson’s disease studies. Published in Nature Communications in 2026, this comprehensive collection represents a pivotal leap toward resolving the complex pathophysiology of Parkinson’s, a condition affecting millions worldwide yet still eluding curative therapies. The iSCORE-PD platform promises to redefine experimental paradigms by providing scientists with genetically matched cellular models that mirror the intricate genetic underpinnings of Parkinson’s disease.

Parkinson’s disease is characterized primarily by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, leading to debilitating motor symptoms such as tremors, rigidity, and bradykinesia, alongside a spectrum of non-motor complications. Despite extensive research, there remains a conspicuous gap between clinical observations and mechanistic understanding at the cellular and molecular levels. Existing animal models and conventional stem cell lines often fall short in recapitulating the exact human pathology. The iSCORE-PD initiative addresses this deficiency head-on by harnessing isogenic stem cell lines, which are genetically identical except for defined Parkinson’s-relevant mutations, thus enabling unprecedented control over genetic variables.

The technical foundation of iSCORE-PD relies on advanced genome editing methodologies, most notably CRISPR/Cas9 technology. By precisely introducing or correcting mutations in key genes implicated in Parkinson’s pathogenesis such as SNCA, LRRK2, PINK1, and PARKIN, researchers have generated isogenic pairs of induced pluripotent stem cells (iPSCs). These iPSC lines can subsequently be differentiated into dopaminergic neurons or other relevant cell types, facilitating side-by-side comparisons that isolate the effects of specific genetic alterations without the confounding noise of inter-individual genetic variability.

One of the remarkable features of the iSCORE-PD collection is its extensive genomic validation pipeline. Whole genome sequencing and transcriptomic analyses are systematically employed to ensure the integrity and authenticity of the edited lines, confirming that off-target effects are minimized and that the genetic landscape conforms precisely to intended edits. This meticulous validation is crucial for downstream experiments intending to dissect subtle cellular phenotypes attributable to Parkinson’s mutations with a high degree of confidence.

The availability of these isogenic cell lines dramatically enhances the fidelity of disease modeling. Scientists can now observe, in real time and within a human cellular context, the cascade of pathological events triggered by individual mutations. For instance, iSCORE-PD lines harboring the G2019S mutation in LRRK2 have already demonstrated distinct lysosomal dysfunction and mitochondrial impairment, hallmarks of Parkinson’s-related neurodegeneration. These insights provide vital clues about the molecular mechanisms that underpin neuronal vulnerability and death.

Beyond mechanistic studies, iSCORE-PD serves as an invaluable platform for drug discovery and therapeutic screening. High-throughput assays conducted on these standardized cellular models allow for robust evaluation of candidate compounds’ efficacy and toxicity. The isogenic background ensures that drug responses can be directly attributed to genetic contributors and not extraneous genomic differences, thereby accelerating the identification of promising therapeutic leads with increased translational potential.

Moreover, the iSCORE-PD repository supports integrative omics approaches. By coupling proteomics, metabolomics, and epigenomic profiling with the genetically defined cell lines, researchers can generate comprehensive molecular atlases elucidating the multifaceted alterations engendered by Parkinson’s-associated mutations. Such data-rich resources augment our understanding of disease heterogeneity and may reveal novel biomarkers for early diagnosis and progression monitoring.

The initiative also pioneers robust methodologies for modeling non-cell autonomous effects in Parkinson’s pathology. By co-culturing isogenic dopaminergic neurons with glial cells or other brain cell types derived from similarly engineered iPSC lines, investigators can explore the cell–cell interactions and inflammatory pathways that contribute to disease propagation. These complex in vitro systems increasingly resemble the in vivo brain microenvironment, bridging translational gaps.

In addition to its scientific hinge, iSCORE-PD represents a significant step forward in reproducibility and collaborative science. By providing open-access to a rigorously characterized and genetically standardized stem cell collection, the project promotes harmonization of experimental models across laboratories worldwide. This standardization mitigates discrepancies often observed in Parkinson’s research due to genetic heterogeneity of patient-derived cells and disparate culture conditions.

Ethical considerations have been front and center in the development and dissemination of the iSCORE-PD lines. The team has implemented stringent protocols to ensure donor anonymity, informed consent, and compliance with international guidelines for stem cell research. This ethical diligence is fundamental to fostering public trust and enabling broad scientific utilization with responsibility.

The iSCORE-PD research consortium envisions future expansion of the collection to encompass additional mutations, gene variants, and epigenetic modifications implicated in Parkinson’s disease, thereby creating an ever-more comprehensive toolkit for the field. This evolving repository will facilitate the study of gene–environment interactions and provide models for the sporadic forms of Parkinson’s that constitute the majority of cases.

Importantly, the development of iSCORE-PD aligns synergistically with advances in single-cell sequencing and live-cell imaging technologies. These combined approaches empower real-time monitoring of neuronal dynamics, synaptic connectivity, and intracellular trafficking in disease-relevant contexts. Such capabilities promise to unravel the temporal progression of neuronal dysfunction in unprecedented detail.

The translational impact of iSCORE-PD extends beyond fundamental research, holding profound implications for personalized medicine. Patient-specific isogenic lines can be derived, enabling evaluation of individualized drug responses and prediction of disease progression trajectories. This precision medicine paradigm could revolutionize clinical management and therapeutic development for Parkinson’s patients.

Finally, iSCORE-PD serves as a testament to the power of interdisciplinary collaboration, integrating expertise in stem cell biology, genome editing, neuroscience, bioinformatics, and clinical neurology. This concerted effort exemplifies how cutting-edge technologies, when harnessed collectively, can illuminate complex diseases and hasten the arrival of effective treatments.

In sum, the iSCORE-PD isogenic stem cell collection stands as a groundbreaking resource that transforms the landscape of Parkinson’s disease research. By providing genetically precise, highly validated cellular models, it enables unparalleled mechanistic insights, drug discovery opportunities, and personalized medicine applications. As the Parkinson’s field grapples with its most urgent challenges, iSCORE-PD promises to be a beacon guiding innovative interventions and ultimately improving patient outcomes worldwide.

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Subject of Research: Parkinson’s disease; isogenic stem cell models; neurodegeneration; genome editing; induced pluripotent stem cells.

Article Title: iSCORE-PD: an isogenic stem cell collection to research Parkinson’s disease.

Article References:

Busquets, O., Li, H., Syed, K.M. et al. iSCORE-PD: an isogenic stem cell collection to research Parkinson’s disease.
Nat Commun (2026). https://doi.org/10.1038/s41467-026-74355-8

Image Credits: AI Generated

Microplastics: Unseen Threats to Liver Health Revealed Through Cutting-Edge Spatial Transcriptomics

In recent years, microplastics have emerged as pervasive environmental contaminants, infiltrating virtually every corner of the globe. These minuscule plastic particles, derived from the breakdown of larger plastic debris, have invaded air, water, and soil, exposing humans to continuous contact via inhalation, ingestion, and dermal absorption. Despite the ubiquity of microplastics, understanding their direct impact on biological systems has remained a formidable challenge within the scientific community. A groundbreaking study by researchers at the University of Oklahoma, recently published in the journal Science Advances, delves into this critical area by examining how microplastics particularly affect liver health under dietary stress conditions.

Tae Gyu Oh, Ph.D., an assistant professor of oncology science at the University of Oklahoma College of Medicine and lead author of the study, highlights the pressing concern: “Exposure to microplastics is inevitable. Their presence in human tissues has been confirmed across multiple studies. However, we wanted to investigate how microplastic exposure interacts with a high-fat, high-cholesterol diet, known to independently induce liver damage.” The study offers compelling evidence that the combination of a typical Western diet and microplastic exposure exacerbates liver injury, potentially accelerating the progression of metabolic liver diseases.

Central to the study is the focus on polyethylene, the most prevalent plastic polymer globally, commonly found in everyday items such as plastic bags and milk containers. The research team administered polyethylene microplastics to mice over eight weeks, with one cohort receiving a standard diet and another subjected to a diet mimicking metabolic dysfunction-associated steatohepatitis (MASH). This severe form of fatty liver disease is characterized by inflammation and liver cell damage, often culminating in cirrhosis and liver failure if untreated.

The findings were striking: mice consuming the high-fat diet alongside microplastic exposure exhibited blood markers indicating liver injury more than twice as elevated as those on a standard diet experiencing similar exposure. This synergistic effect underscores the intricate interplay between environmental pollutants and diet-induced metabolic stressors, intensifying hepatic damage beyond what each factor causes independently.

To unravel the molecular and cellular underpinnings of this phenomenon, the research employed an array of sophisticated analytical techniques, culminating in the use of spatial transcriptomics. Unlike conventional bulk transcriptomic approaches, which average gene expression across millions of cells and can obscure localized responses, spatial transcriptomics enables researchers to map transcriptional activity within intact tissue sections at near single-cell resolution. This technique revealed precise “hot spots” of inflammation and tissue injury within the liver, a breakthrough insight unattainable by earlier methodologies.

Analysis of gene regulatory networks through spatial transcriptomics indicated a pivotal role for PPAR-alpha (peroxisome proliferator-activated receptor-alpha), a nuclear receptor that orchestrates fat metabolism and energy homeostasis in liver cells. PPAR-alpha appears to engage in cross-talk with Anxa2, a gene implicated in tissue repair and membrane dynamics. The altered activity of this axis in microplastic-exposed livers suggests that microplastics may disrupt the liver’s natural defense and regenerative processes, impairing its capacity to recover from metabolic insults.

This discovery has profound implications for understanding the mechanistic pathways by which environmental contaminants like microplastics contribute to liver pathology. The perturbation of PPAR-alpha and Anxa2 signaling potentially links microplastic exposure with the dysregulation of lipid metabolism and compromised repair, exacerbating the severity of conditions such as nonalcoholic fatty liver disease (NAFLD) and MASH.

While these findings were generated in a murine model, they establish an essential framework that informs potential human health risks. Given the parallels between murine and human liver physiology, it is plausible that microplastic exposure combined with high-fat diets could similarly predispose humans to aggravated liver damage. However, the researchers caution that further studies are necessary to confirm this translation and to elucidate the long-term implications for populations worldwide.

Dr. Oh emphasizes the broader relevance of this research: “Microplastics are now inextricably linked to daily life, yet their biological impact is only beginning to be understood. Through advanced spatial transcriptomic mapping, we have visualized the precise loci of hepatic damage induced by microplastics, revealing a novel environmental dimension to liver disease pathogenesis.” This nuanced comprehension paves the way for future investigations targeting environmental and dietary risk factors in liver health.

Moreover, these insights open avenues for therapeutic targeting. Modulating the PPAR-alpha-Anxa2 pathway could become a strategy to mitigate microplastic-induced liver injury or fortify the liver’s resilience against environmental toxins. Understanding such molecular crosstalk also facilitates improved diagnostic markers sensitive to environmental damage, allowing for earlier intervention in vulnerable populations.

This pioneering study exemplifies the intersection of environmental health, genomics, and hepatology, demonstrating how innovative technologies can elucidate complex biological interactions. It underscores the urgent need to address microplastic pollution not only as an ecological crisis but as a public health priority, particularly in societies where high-fat diets are prevalent.

As humanity grapples with escalating plastic waste and its fragmentary descent into invisible pollutants, research such as this serves as a clarion call for comprehensive strategies. Reducing plastic production, enhancing waste management, and fostering healthier dietary practices collectively form the cornerstone of mitigating hidden dangers to liver health and overall well-being.

The University of Oklahoma study, titled “Spatial Transcriptome Mapping Identifies Ppara-Anxa2 Crosstalk in Microplastic-Induced Hepatotoxicity,” stands as a seminal contribution offering unprecedented mechanistic clarity. Through employing spatial transcriptomics, the researchers have achieved a level of resolution that redefines how environmental toxicology and metabolic disease research can coalesce to confront emergent health threats posed by our plastic-saturated environment.

Subject of Research: Animals
Article Title: Spatial transcriptome mapping identifies Ppara-Anxa2 cross-talk in microplastic-induced hepatotoxicity
News Publication Date: 17-Jun-2026
Web References: https://doi.org/10.1126/sciadv.aec8681
References: Oh, T.G., Jung, W., Joshi, A.D., et al. Spatial Transcriptome Mapping Identifies Ppara-Anxa2 Crosstalk in Microplastic-Induced Hepatotoxicity. Science Advances, 2026.
Image Credits: University of Oklahoma
Keywords: Microplastics, Liver Disease, Fatty Liver Disease, Polyethylene, High-Fat Diets, Spatial Transcriptomics, PPAR-alpha, Anxa2, Hepatotoxicity, Environmental Health, Metabolic Dysfunction, Inflammation

Emerging insights into autism spectrum disorder (ASD) have been propelled forward by an innovative study examining cortical development dynamics using multiple mouse models. This work delves deeply into the transcriptional landscapes shaped by mutations implicated in ASD, revealing a complex interplay of stage-specific and genotype-specific molecular signatures. Employing cutting-edge network colocalization analyses and protein–protein interaction mapping, the study illuminates how biological processes converge and diverge during neurodevelopment in mutant genotypes.

Fundamentally, the research builds upon gene set enrichment analysis (GSEA), which previously highlighted overlapping pathways across various ASD-related mutations. The researchers expanded on this by applying network colocalization analysis to protein interaction networks, allowing functionally related proteins to be grouped into clusters through sophisticated averaging of random walks. This methodological advancement enables a nuanced assessment of expression changes aggregated at the systems-level rather than focusing solely on individual genes.

At the heart of their findings is the identification of distinct yet overlapping patterns of molecular dysregulation during critical developmental stages, particularly embryonic day 14.5 (E14.5), postnatal day 4 (P4), and postnatal day 14 (P14). At E14.5, the study reveals that mutations such as those in HnrnpU and Kdm6b robustly influence pathways tied to the actin cytoskeleton, cell proliferation, and division within excitatory neurons. Notably, these effects also extend, to a lesser degree, to Cul3 mutants, aligning with earlier evidence suggesting these genes’ involvement in neurodevelopmental regulation.

Delving deeper, the analysis highlights a provocative role of WNT signaling, especially pronounced in HnrnpU and Kdm6b variants. WNT pathways are critical for neural patterning and synaptogenesis, and their disruption could underpin some ASD phenotypes. This novel perspective accentuates the shared mechanistic underpinnings of ASD mutations converging on fundamental developmental pathways, stressing the importance of timing within neurodevelopmental trajectories.

Postnatally, at P4 and P14, the transcriptional alterations shift noticeably towards synaptic functions, ion transport, and metabolic processes—markers of neuronal specialization and circuit maturation. The data demonstrate how the influence of mutations evolves alongside neural differentiation and maturation. Intriguingly, Kmt5b mutants exhibited an inverse pattern at P4, suggesting either a compensatory or opposing regulatory role within the shared pathways affected across mutants. This counterintuitive finding raises the possibility of complex feedback or adaptive mechanisms operating in ASD-linked genetic variants.

By P14, metabolic processes prominently emerge in the affected molecular networks, especially in Bckdk, HnrnpU, and Trip12 mutants, indicating that energy metabolism perturbations may be integral to ASD pathogenesis. These results underscore the temporal dynamics of how genetic mutations impinge upon neurodevelopment, transitioning from early cytoskeletal and proliferative effects to later synaptic and metabolic modulation.

The study also innovatively explores how differentially expressed genes from each genotype localize within the interactome network and assesses similarity across developmental stages and mutations. This reveals a compelling developmental-stage-dependent pattern where transcriptional signatures cluster more closely within each stage but become more genetically distinct by P14. Such divergence suggests that while ASD mutations initially impact common biological processes, their influence fragments into distinct genotype-specific programs as development proceeds.

These findings have broad implications for understanding ASD heterogeneity and the challenges of developing universal therapeutic interventions. The discovery of both shared and unique pathway disruptions at different developmental times suggests treatment strategies may need to be tailored to both genotype and developmental timing to maximize efficacy. Moreover, the role of metabolic dysregulation invites further exploration into metabolic interventions or dietary modulation as adjunctive strategies.

Critically, the network colocalization analysis used represents a powerful approach to dissecting complex genetic disorders. By moving beyond simple gene expression differences and integrating system-level interactions, researchers can better capture the multifaceted nature of neurodevelopmental perturbations characteristic of ASD. This systems biology approach is likely to prove invaluable in future studies dissecting the molecular bases of brain disorders.

The comprehensive nature of this study, which integrates multiple ASD-relevant mouse models, enables the identification of convergent and divergent mechanisms with precision. It highlights how individual genes implicated in autism can distinctly alter transcriptional landscapes depending on context, highlighting the multifactorial dimension of ASD. Additionally, it underscores that the timing of gene dysregulation is paramount, with early embryonic disruptions cascading into diverse neurodevelopmental consequences.

In sum, this landmark investigation offers a rich, dynamic map of the molecular trajectories altered by ASD mutations across cortical development. Its integration of genomic, proteomic, and network analyses provides a blueprint for future research aimed at unraveling the complexity of neurodevelopmental disorders. By elucidating how multiple risk genes influence overlapping yet unique biological processes during critical developmental windows, the study charts a path toward precision medicine in autism spectrum disorder.

As the field progresses, leveraging such multi-dimensional analytical frameworks will be essential for translating genetic discoveries into mechanistic insights and targeted therapies. This work also highlights the ongoing need to examine neurodevelopment through temporal and molecular lenses simultaneously, enriching our understanding of how genetic diversity shapes brain development and function. Ultimately, investigations like these nurture hope for deciphering the intricate biology underlying ASD and devising effective interventions tailored to individual developmental trajectories.

Subject of Research: Cortical development dynamics and molecular mechanisms in autism spectrum disorder mouse models.

Article Title: Cortical development dynamics across autism spectrum disorder mouse models.

Article References:
Schwarz, L.A., Dotter, C.P., Isaev, S. et al. Cortical development dynamics across autism spectrum disorder mouse models. Nature (2026). https://doi.org/10.1038/s41586-026-10679-1

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41586-026-10679-1

In a groundbreaking advancement in the treatment of metastatic urothelial cancer, a recent clinical trial has explored the synergistic potential of combining immune checkpoint inhibitors tremelimumab and durvalumab with the chemotherapeutic agent paclitaxel. This phase I/II ICRA trial, published in the prestigious Nature Communications, offers compelling evidence that dual immune modulation with or without chemotherapy may redefine therapeutic paradigms for this challenging malignancy. The innovative study meticulously investigates the safety profile, optimal dosing, and preliminary efficacy signals of these agents when administered simultaneously, charting a promising new course in oncologic therapeutics.

Urothelial carcinoma, predominantly affecting the bladder, represents a formidable oncological challenge due to its aggressive nature and propensity for metastasis upon progression. While immune checkpoint inhibitors have revolutionized cancer care by unleashing the host’s immune system against tumor cells, their efficacy as monotherapy in advanced urothelial cancer remains variable. Tremelimumab, a monoclonal antibody targeting CTLA-4, and durvalumab, an anti-PD-L1 antibody, function by disrupting distinct immunosuppressive pathways that tumors exploit to evade immune detection. The rationale behind combining these agents with paclitaxel—a cytotoxic drug known for interfering with microtubule dynamics—lies in the complementary mechanisms that might potentiate antitumor responses.

The trial enrolled patients with histologically confirmed metastatic urothelial cancer who had exhausted or were ineligible for standard therapeutic options. Participants received varying regimens comprising tremelimumab alone, tremelimumab plus durvalumab, and either combination with paclitaxel. This design sought to delineate the safety thresholds and dose-limiting toxicities while enabling exploratory analyses of clinical outcomes such as progression-free survival and objective response rates. Detailed immune profiling and biomarker assessments accompanied the clinical evaluations to decipher correlates of response and resistance.

Initial data reveal that the combination treatments are generally well tolerated, with adverse events consistent with known profiles of checkpoint inhibitors and chemotherapy. Immune-related adverse events—such as dermatitis, colitis, and endocrinopathies—were manageable within established guidelines, emphasizing the importance of vigilant monitoring and timely intervention. Importantly, no unexpected synergistic toxicities emerged, suggesting that these agents can be safely coadministered without exacerbating systemic toxicity.

From an efficacy standpoint, tremelimumab combined with durvalumab and paclitaxel demonstrated encouraging antitumor activity, surpassing response rates historically observed with any single agent in this patient cohort. Objective responses included significant tumor burden reductions, with some patients experiencing durable disease stabilization or partial remission. Notably, the addition of paclitaxel appeared to enhance immunogenic cell death, potentially promoting antigen presentation and T-cell activation, thus amplifying the therapeutic window of the checkpoint blockade.

Correlative translational studies provided insights into the immunological milieu shaping treatment responses. Tumor biopsies and peripheral blood analyses highlighted increased infiltration of CD8+ cytotoxic T lymphocytes and a concomitant decrease in immunosuppressive regulatory T cells in responders. Furthermore, upregulation of interferon-gamma signaling pathways and enhanced expression of antigen processing machinery were observed, aligning with the hypothesis that chemotherapy-induced immunogenicity synergizes with checkpoint inhibition to invigorate antitumor immunity.

Another pivotal observation was the heterogeneity in patient outcomes, underscoring the necessity for biomarker-driven patient stratification. Molecular profiling identified tumor mutational burden and PD-L1 expression levels as potential predictive biomarkers, although their roles require further validation. Intriguingly, emerging evidence suggests that tumor microenvironment features—such as cytokine profiles and myeloid cell populations—may also influence responsiveness, opening new avenues for personalized immunotherapy approaches.

The trial’s phased escalation design allowed for adaptive modifications based on interim results, optimizing dosing regimens to balance efficacy and safety. These methodological strengths enhance the reliability of conclusions drawn and set a precedent for future combination trials in urothelial carcinoma and beyond. Additionally, pharmacokinetic analyses confirmed that neither agent significantly altered the metabolism of the others, supporting their compatibility in combination therapies.

This landmark investigation contributes critical knowledge to the evolving landscape of bladder cancer treatment by demonstrating how rationally designed combinations of immune checkpoint inhibitors and chemotherapies can elicit potent antitumor effects in metastatic disease. Given the historically poor prognosis for advanced urothelial cancer, these findings herald a new era where multi-agent immunomodulation may offer renewed hope for patients. However, broader phase III studies will be essential to confirm survival benefits and thoroughly characterize long-term safety.

Moreover, the translational components embedded within this study exemplify the growing trend towards integrating laboratory science with clinical oncology. Such integrative approaches are crucial for unraveling the complex interplay between tumor biology and therapeutic interventions, ultimately facilitating the development of more effective, tailored treatments. The ICRA trial represents an exemplar of precision medicine in action, advancing beyond one-size-fits-all approaches towards nuanced, biomarker-informed strategies.

While the current research focuses on metastatic urothelial carcinoma, the implications extend to other malignancies where immune evasion is a critical obstacle. The dual blockade of CTLA-4 and PD-L1 pathways in concert with chemotherapeutic agents may prove universally applicable, prompting parallel investigations across diverse cancer types. Furthermore, understanding the mechanisms that underlie response and resistance could inform the design of next-generation immunotherapies, including combination regimens incorporating novel agents such as oncolytic viruses, vaccines, or cell-based therapies.

In the broader context of cancer immunotherapy, the trial reinforces the concept that combining immune checkpoint inhibitors with traditional cytotoxic chemotherapy can create a more hostile environment for cancer cells while simultaneously activating immune effector functions. This synergistic interaction leverages the strengths of both modalities: chemotherapy disrupts tumor cell replication and induces immunogenic cell death, while checkpoint inhibitors relieve inhibitory signals that dampen T-cell activity. Together, they orchestrate a multifaceted assault on cancer.

The success of this approach depends heavily on careful patient selection, vigilant management of immune-related adverse events, and comprehensive biomarker development. As immune therapies increasingly become standard in oncology, multidisciplinary collaborations between clinicians, immunologists, and computational biologists will be vital to fully harness their potential. The ICRA trial epitomizes such collaborative effort, merging clinical expertise with cutting-edge immunological research.

In summary, the phase I/II ICRA trial investigating tremelimumab with or without durvalumab in combination with paclitaxel in metastatic urothelial cancer delineates a compelling therapeutic strategy blending checkpoint blockade and chemotherapy. It underscores important principles regarding safety, efficacy, and mechanistic synergy while illuminating paths for future exploration. As the oncology community eagerly awaits results from larger confirmatory studies, this trial stands as a milestone in the continuous quest to improve outcomes for patients facing this formidable disease.

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Subject of Research: Combination immunotherapy with tremelimumab and durvalumab alongside paclitaxel chemotherapy in metastatic urothelial cancer.

Article Title: Tremelimumab with or without durvalumab in combination with paclitaxel in metastatic urothelial cancer: phase I/II ICRA trial.

Article References: Einerhand, S.M.H., Ali, H., Wong, S.Q. et al. Tremelimumab with or without durvalumab in combination with paclitaxel in metastatic urothelial cancer: phase I/II ICRA trial. Nat Commun (2026). https://doi.org/10.1038/s41467-026-74570-3

Image Credits: AI Generated

In a landmark achievement for cardiovascular care, one hundred hospitals across the United States have been awarded the prestigious American College of Cardiology (ACC) HeartCARE Center designation. This recognition represents the pinnacle of commitment to delivering superior, patient-centered cardiovascular treatment. Introduced in 2018, the HeartCARE Center designation is the ACC’s most esteemed accolade for hospitals and health systems, acknowledging institutions that exhibit sustained clinical excellence through comprehensive accreditation, rigorous performance monitoring via data analytics, and ongoing quality improvement processes.

This milestone reflects the ACC’s unwavering dedication to advancing the standards by which cardiovascular services are delivered nationwide. The hospitals recognized demonstrate adherence to evidence-based clinical protocols, participation in continuous quality enhancement initiatives, and the achievement of measurable patient outcomes that transcend regional disparities. Steven B. Deitelzweig, MD, MMM, FACC, chair of the ACC Accreditation Oversight Committee, emphasized the significance of this accomplishment, highlighting that these institutions collectively enhance cardiovascular care quality, ensuring access for patients wherever they reside.

The HeartCARE Center designation is conferred upon organizations that meet stringent criteria encompassing participation in a minimum of two ACC Accreditation Services programs and engagement with National Cardiovascular Data Registry (NCDR) registries. These registries serve as pivotal platforms for tracking and benchmarking clinical outcomes, enabling hospitals to pinpoint and bridge gaps in guideline-based care implementation. Furthermore, targeted quality improvement campaigns such as the Patient Navigator Program: Focus MI support institutions in closing those gaps through structured, scientifically grounded interventions.

Beyond accreditation and registry participation, the HeartCARE Center program integrates robust continuous performance measurement mechanisms. This integration fosters a culture of accountability and data-driven decision-making within hospitals, enabling them to consistently execute guideline-directed care pathways. The approach is designed not only to improve clinical outcomes for cardiovascular patients but also to enhance process efficiency and interprofessional collaboration across care teams, thereby standardizing high-quality care delivery throughout participating institutions.

As an integral component of the ACC’s broader Quality Improvement for Institutions initiative, the HeartCARE Center designation symbolizes organizational leadership in sustainable quality improvement. These hospitals exemplify best practices in process optimization, specialty-specific accreditation, clinical staff development, and active engagement with their surrounding communities. Collectively, these elements work synergistically to establish a new benchmark for coordinated, patient-centered cardiovascular care, expanding patient access to state-of-the-art heart health interventions locally.

By earning the HeartCARE Center designation, hospitals demonstrate not just isolated achievements but a persistent commitment to maintaining and advancing quality care across the entire spectrum of cardiovascular medicine. Dr. Deitelzweig noted that the rigorous standards required for designation translate into tangible benefits for patients, including improved survival rates, reduced complication incidences, and broader availability of the latest evidence-supported therapies. This systematic elevation of care quality promises to transform cardiovascular outcomes on a national scale.

The ACC’s strategic emphasis on integrating data from accreditation services and NCDR registries enables participating institutions to continuously refine clinical protocols in response to emerging evidence and outcome trends. This data-centric framework underpins the excellence recognized by the HeartCARE Center program, equipping hospitals with actionable insights for enhancing care pathways, reducing practice variability, and advancing the science of cardiovascular treatment delivery.

Technological advancements and sophisticated analytics play central roles in this process improvement paradigm. The ability to harness large-scale clinical data sets from the NCDR registries facilitates risk-adjusted benchmarking, enabling institutions to evaluate performance relative to national standards. This capability supports precision targeting of quality improvement efforts—ensuring resources are effectively allocated to areas with the greatest potential to impact patient care outcomes.

Community outreach and patient engagement initiatives are further hallmarks of HeartCARE Centers. These institutions not only excel internally but also proactively extend their knowledge and services beyond hospital walls. By fostering partnerships with local health organizations and enhancing public health education, HeartCARE Centers contribute to the prevention and early detection of cardiovascular disease, thereby addressing systemic health disparities and promoting holistic cardiovascular wellness.

Moreover, the multidisciplinary nature of cardiovascular care teams within HeartCARE Centers underscores the program’s emphasis on comprehensive treatment. Cardiologists, cardiac surgeons, nurses, rehabilitation specialists, and other healthcare professionals collaborate seamlessly to deliver continuity of care that is responsive to individual patient needs. This integrated care model has been shown to enhance adherence to treatment plans, improve functional recovery, and reduce hospital readmission rates.

Sustained professional education and credentialing efforts complement these clinical advancements, ensuring that healthcare providers within HeartCARE Centers remain at the forefront of cardiovascular medicine. The ACC’s broader infrastructure supports these goals through its renowned JACC journals, certification programs, and educational symposia, cultivating a workforce primed to apply innovative therapies grounded in rigorous scientific evidence.

Collectively, the achievement of 100 HeartCARE Center designations signals a transformative moment for cardiovascular care delivery in the United States. The program’s emphasis on data-driven quality improvement, comprehensive accreditation, and community-centered care sets a new standard that other healthcare disciplines may emulate. As more hospitals join the ranks of HeartCARE Centers, patients nationwide stand to benefit from enhanced outcomes, greater consistency in treatment, and access to cutting-edge, guideline-based cardiovascular therapies.

For those interested in reviewing the complete listing of hospitals designated as ACC HeartCARE Centers, further information is accessible through the ACC’s official platform. This transparency aids healthcare leaders, clinicians, and patients alike in identifying centers that exemplify clinical excellence and serves to incentivize continued quality advancements in cardiovascular medicine.

The American College of Cardiology remains steadfast in its mission to transform cardiovascular care globally. With a community exceeding 60,000 cardiovascular professionals across more than 140 countries, the ACC drives innovation, education, and advocacy, dedicated to optimizing heart health outcomes through scientific rigor and clinical leadership. The HeartCARE Center designation exemplifies this mission, heralding a future in which standardized, high-quality cardiovascular care is universally accessible.

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News Publication Date: Not specified in the source content.

Web References: https://cvquality.acc.org/accreditation/heartcare-center-recognition-program/participating-facilities

Keywords: Cardiovascular care, HeartCARE Center designation, American College of Cardiology, ACC Accreditation, Quality Improvement, NCDR registries, Patient-centered care, Evidence-based treatment, Cardiovascular outcomes, Clinical excellence, Data-driven healthcare, Cardiology hospitals

A groundbreaking hospital-based study conducted in India sheds new light on the complex and often controversial relationship between lifestyle factors and prostate cancer risk. Published in the April 28, 2026 issue of Oncoscience, this investigation provides intriguing evidence that certain modifiable habits, specifically coffee and meat consumption, may significantly reduce the likelihood of developing prostate cancer among men. This revelation emerges despite prostate cancer being the world’s second most prevalent malignancy in men and a critical contributor to cancer-related mortality.

The research was spearheaded by Maya Kulshekar and Anuradha B. Patil at the Department of Biochemistry, Jawaharlal Nehru Medical College, part of the KLE Academy of Higher Education and Research in Karnataka, India. Their work comes at a crucial moment when the incidence of prostate cancer in India is poised to rise markedly, underscoring the urgent need to identify interventions grounded in modifiable risk behaviors.

In this rigorously designed study, 72 men with histopathologically confirmed prostate cancer were compared to 132 control individuals diagnosed with benign prostatic hyperplasia (BPH). The investigators carefully examined a suite of lifestyle factors—ranging from tobacco use and alcohol consumption to dietary patterns including tea, coffee, and meat intake, as well as occupational exposure linked to farming. Thorough multivariate logistic regression analyses allowed the team to adjust for confounding variables, thereby refining the associations between these factors and prostate cancer risk.

The findings revealed a striking inverse association between coffee consumption and prostate cancer risk, translating to an approximate 65% reduction in odds after adjustment for potential confounders. Meat consumption similarly demonstrated a protective effect, associated with a roughly 48% decreased risk. These results challenge some conventional nutritional beliefs and highlight the nuanced role diet may play in modulating prostate oncogenesis.

Contrastingly, the study found no statistically significant correlation between alcohol consumption, tobacco chewing, smoking, tea intake, or farming-related occupational exposure and prostate cancer once confounding factors were accounted for. Initial univariate analyses suggested elevated risk linked to smoking and tobacco chewing; however, these associations dissipated under multivariable scrutiny, suggesting the potential influence of other interacting factors.

The biochemical mechanisms underpinning these associations were thoughtfully explored by the authors. Coffee is a complex beverage rich in bioactive compounds including caffeine, cafestol, kahweol, and a spectrum of antioxidant polyphenols. These molecules have been extensively studied for their anti-inflammatory and antioxidant properties, implicating them in pathways that may suppress malignant transformation or tumor progression. Their capacity to modulate cellular stress responses, DNA repair, and immune regulation positions coffee as a potent functional food in cancer prevention paradigms.

Similarly, meat contains constituents such as trans-vaccenic acid, an unsaturated fatty acid that has been observed in some experimental models to influence immune responses and cellular signaling pathways relevant to oncogenesis. Notwithstanding, the study authors caution that the protective role of meat is complicated by the heterogeneity inherent in types of meat, cooking methods, and quantity consumed—parameters that were not stratified in this investigation. The metabolic and molecular consequences of processed versus unprocessed meats or the generation of carcinogenic compounds during certain cooking processes remain pivotal confounders warranting further rigorous examination.

This research importantly acknowledges the broader scientific context where prior epidemiological studies have reported inconsistent and at times contradictory findings regarding coffee, meat, tobacco, tea, and alcohol in relation to prostate cancer risk. This inconsistency may stem from differences in study design, dietary assessment methods, population genetics, and environmental factors across cohorts. The current study’s contribution lies in focusing on an Indian population, thereby addressing a geographic and ethnic gap in the literature.

The methodological design, while robust, is not without limitations. The single-center hospital-based sample, and relatively modest cohort size, may affect the generalizability of the findings. Additionally, potential recall bias in self-reported lifestyle habits and the absence of quantitative dietary intake measures restrict the granularity of exposure assessment. The authors advocate for larger, multicenter, and longitudinal studies with comprehensive dietary and lifestyle quantification to validate and expand upon these preliminary observations.

This investigation marks an important step toward understanding how modifiable lifestyle factors could temper the risk of prostate cancer. By highlighting coffee and meat intake as potentially protective, the study invites a reevaluation of dietary guidelines and preventive oncology strategies within the Indian context and beyond. The mechanistic insights further fuel the search for bioactive compounds that could be leveraged in therapeutic or nutraceutical formulations.

Ultimately, these findings reinforce the imperative for personalized medicine approaches that integrate lifestyle, genetic, and environmental data to optimize cancer prevention and management. They also echo broader calls within the oncological community to pursue open-access, multidisciplinary research that bridges molecular science with public health imperatives.

While the findings demand cautious interpretation, they open an exciting avenue for leveraging everyday dietary choices as part of a comprehensive prostate cancer risk reduction strategy. As prostate cancer incidence is projected to escalate, especially in rapidly modernizing societies, these insights provide a timely beacon for clinicians, researchers, and policy makers alike.

The study’s implications extend beyond prostate cancer, emphasizing a holistic perspective on how complex interplays of diet, lifestyle, and biological mechanisms coalesce to impact carcinogenesis. It epitomizes the potential for traditional epidemiological research, augmented by advanced statistical modeling, to generate actionable knowledge that may ultimately improve patient outcomes on a population scale.

Researchers and clinicians interested in this expanding field are encouraged to follow ongoing and future work from this team and related cohorts worldwide, as the quest to decipher modifiable risk factors of prostate cancer continues to gain precision and impact.

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Subject of Research: People
Article Title: Modifiable risk factors of prostate cancer: Insights from a hospital-based study
News Publication Date: 28-Apr-2026
Web References: https://doi.org/10.18632/oncoscience.657
Image Credits: Copyright © 2026 Kulshekar et al. Creative Commons Attribution License (CC BY 4.0)
Keywords: modifiable risk factors, prostate cancer, awareness, India, molecular mechanism

In a groundbreaking study that redefines our understanding of how language is encoded in the human brain, researchers have mapped the diverse landscape of neurons distributed across frontal and temporal cortical regions, revealing a complex yet lateralized neural architecture for human language processing. By leveraging advanced single-neuron recording techniques alongside sophisticated language models, the team has identified not just the locations but the nuanced encoding properties of neurons implicated in various linguistic computations. This work illuminates how language, a uniquely human faculty, is instantiated at the neuronal level with precision and regional specificity.

The study’s comprehensive neuronal recordings spanned key brain areas historically associated with language, including the frontal cortex, anterior temporal cortex, and posterior temporal cortex. These regions were chosen given their established roles in speech production and linguistic comprehension, as well as their demonstrated selective responses in prior localized brain imaging studies. Importantly, the neurons examined were broadly distributed across both hemispheres and these cortical regions, showcasing the widespread neural substrate involved in language tasks.

One of the seminal findings was that roughly half of the neurons, 289 out of 579, exhibited selective responsiveness to one or more linguistic features. Intriguingly, this selectivity was evenly distributed across the three cortical sites — frontal, anterior temporal, and posterior temporal — and did not significantly differ between the left and right hemispheres. This suggests a foundational neural scaffold where language-related computations recruit a multitude of neurons across large-scale networks rather than isolated hotspots, emphasizing distributed processing over modular localization.

However, beyond this broad distribution, the study uncovered striking lateralization and regional differentiation in the strength and informational content of neural modulation. Neurons within the left hemisphere exhibited significantly stronger modulation—quantified by their z-scored activity changes—in response to linguistic features compared to their right hemisphere counterparts. This enhanced sensitivity encompassed a range of linguistic elements, including lower-order features like pitch, underscoring the superior role of the left hemisphere in detailed linguistic encoding.

Further dissecting these lateralized effects across cortical regions revealed that the posterior temporal cortex showed the most pronounced difference in left-right modulation strength, significantly outperforming other areas. This aligns well with the notion that posterior temporal areas are central to decoding complex linguistic dependencies and syntactic structures, functions critical for fluent language comprehension and production.

Conversely, the prefrontal cortex displayed the strongest overall neuronal modulation to these language features, both in the left and right hemispheres, compared to temporal regions. This finding suggests a hierarchical and possibly integrative role for the frontal cortex in orchestrating language processing, perhaps linked to higher-order syntactic planning, working memory, or executive control mechanisms required for natural speech.

The neural predictivity analysis, leveraging embeddings from cutting-edge contextual language models, further corroborated the lateralized and regionalized pattern. Neural activity in the left anterior temporal cortex was most accurately predicted by these language model features, highlighting this region’s role in abstract linguistic representation and semantic integration during language tasks.

Methodologically, the study capitalized on the precise temporal resolution of single-neuron recording combined with sophisticated statistical analyses, including permutation and rank-sum tests, to quantify neuronal response selectivity and modulation. This rigorous approach afforded a fine-grained characterization of how individual neurons adapt their firing patterns to various syntactic and prosodic elements of language in real-time.

Collectively, these data challenge conventional notions that neural language processing is confined to narrowly defined “language centers.” Instead, the findings advocate for a model of language representation as a widely distributed but regionally specialized system with marked hemispheric dominance. This has profound implications for understanding the neural basis of language disorders, suggesting that therapeutic interventions might need to consider both distributed network integrity and hemispheric targeting.

Moreover, the study’s integration of naturalistic language models with neurophysiological data marks a pioneering step in computational neuroscience, bridging theoretical frameworks of language with tangible neural mechanisms. By showing how models trained solely on linguistic input can approximate neuronal responses, this research points toward a future where artificial intelligence and neuroscience synergistically unravel human cognition.

Importantly, the results underscore the unique neural architecture supporting language that has evolved in humans, outstripping earlier simplistic models focused on gross anatomical mapping. These advances set the stage for future investigations that might explore how these neuronal populations interact dynamically during complex language tasks such as conversation, narrative comprehension, or bilingual processing.

In conclusion, this landmark research paints a detailed, high-resolution portrait of the neuronal building blocks underpinning human language. It reveals an exquisitely lateralized and regionally differentiated system whereby distributed neurons collectively encode the multifaceted features of speech. Such insights not only deepen fundamental neuroscience but also hold promise for novel clinical interventions and computational linguistic advancements.

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Subject of Research: Neuronal encoding of human language features across frontal and temporal cortical regions; lateralization and regional differentiation of linguistic processing in the brain.

Article Title: Mapping the neuronal building blocks of human language with language models.

Article References:
Cai, J., Kfir, Y., Jamali, M. et al. Mapping the neuronal building blocks of human language with language models. Nature (2026). https://doi.org/10.1038/s41586-026-10691-5

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41586-026-10691-5