'; ?> geneimprint : Hot off the Press http://www.geneimprint.com/site/hot-off-the-press Daily listing of the most recent articles in epigenetics and imprinting, collected from the PubMed database. en-us Thu, 11 Jun 2026 14:45:34 EDT Thu, 11 Jun 2026 14:45:34 EDT jirtle@radonc.duke.edu james001@jirtle.com Arsenic exposure at birth, socioeconomic status, and epigenetic aging among adults in northern Chile. Kwon D, Bozack AK, Ferreccio C, McCormick N, Steinmaus CM, de la Rosa R, Cardenas A
Environ Res (Jun 2026)

Arsenic exposure remains a major global health concern, and early-life exposure has been linked to cancer, cardiovascular disease, and diabetes. Epigenetic biomarkers of aging may capture long-term effects of arsenic, yet whether exposure during sensitive developmental windows leaves detectable epigenetic signatures decades later remains unclear. Socioeconomic status (SES) may modify these relationships, yet its role as a modifier has not been examined.]]> Wed, 31 Dec 1969 19:00:00 EST The transformative role of single-cell analysis in multifactorial disorders research. Wang CY, Ko CC, Kumar S, Xuan DTM, Lin HR, Lee YK, Nguyen NUN, Yang PM, Solomon DD
Methods (Jul 2026)

Multifactorial inherited disorders (MIDs) arise from complex interactions between polygenic risk and environmental exposures, presenting major challenges for mechanistic discovery, patient stratification, and targeted therapy development. While traditional approaches like genome-wide association studies (GWAS) and bulk omics profiling have identified broad associations, they often struggle to resolve the cellular context in which these interactions drive pathogenesis.Emergingsingle-cell technologies now offer unprecedented resolution to dissect tissue heterogeneity, define rare or transient disease-relevant cell states, and map dynamic trajectories across tissues and disease stages. This reviewprovides a comprehensive synthesis ofcurrent single-cell methodologies including transcriptomic, epigenomic, proteomic, and spatial techniques and their application to MID research. We explore how these toolsare revealingcell-type-specific regulatory circuits,contextualizingthe functional impact of inherited risk variants, andelucidatingcellular responses to environmental perturbations.We propose thatintegrating single-cell multi-omics data is critical for illuminating the mechanistic basis of complex traits and for advancing biomarker discovery. However, significant challenges remain, including technical variability, limited cohort scalability, difficulties in multi-modal data integration, and a lack of standardized analytical workflows for polygenic diseases. Overcoming these barriers will require harmonized study designs, robust computational frameworks, and the incorporation of longitudinal and environmental exposure data.Ultimately, we conclude thatsingle-cell analysis is poised to transform MID research, offering a powerful new paradigm for mechanistic insight, therapeutic innovation, and the realization of precision medicine.]]> Wed, 31 Dec 1969 19:00:00 EST Interactions between nutrition and the epigenome: how can it be harnessed for public health? Anastasopoulou M, Dereki I, Sgourou A, Lagoumintzis G
Future Sci OA (Dec 2026)

A substantial body of evidence shows that dietary habits influence gene expression and epigenetic processes, holding significant implications for public health policies. Epigenetic modifications are increasingly associated with metabolic state, disease risk, and biological aging. Translating mechanistic results into scalable, efficient nutritional epigenetics treatments is difficult.]]> Wed, 31 Dec 1969 19:00:00 EST Omics-driven strategies for identifying biomarkers in Alzheimer's disease. Khan Y, Rekha A, Ballal S, Maharana L, Maqbool M, Goyal K, Mishra R, Uniyal P, Alam P, Aljarba TM, Gupta G, Hussain MS
Metab Brain Dis (Jun 2026)

Alzheimer's disease (AD) is a progressive neurodegenerative disorder with limited treatment options, mainly due to late diagnosis and partial understanding of its molecular aspects. Traditional biomarker discovery approaches have significantly contributed to AD diagnostics but suffer from limitations. The advent of omics technologies (genomics, epigenomics, transcriptomics, proteomics, and metabolomics) has revolutionized the search for novel biomarkers by enabling comprehensive molecular profiling. Genomic studies have identified risk-associated variants such as APOE4, while epigenomic alterations, including DNA methylation alterations, offer insight into gene regulation in AD. Transcriptomic analyses, particularly single-cell and spatial transcriptomics, have uncovered molecular pathways linked to neuroinflammation and synaptic dysfunction. Proteomic advancements, including mass spectrometry and extracellular vesicle profiling, have identified potential blood- and CSF-based biomarkers for early-stage detection. Metabolomic and lipidomic studies indicate that cerebral glucose hypometabolism, insulin resistance, mitochondrial damage, redox imbalance, and disrupted lipid homeostasis are centra contributors to AD pathogenesis rather than secondary considerations of the disease. These metabolic dysfunctions may precede overt neurodegeneration and influence amyloid processing, tau phosphorylation, neuroinflammatory activation, and synaptic loss, thereby generating clinically informative biomarker signatures in blood and cerebrospinal fluid. Within this metabolism-centered paradigm, integrative multi-omics approaches are particularly valuable because they not only enhance biomarker specificity, but also connect molecular signatures with bioenergetic and immune-mediated mechanisms of disease. Accordingly, integrative multi-omics approaches improve biomarker specificity and predictive power, thereby supporting the development of precision medicine and targeted therapeutic interventions. Nevertheless, important challenges remain, including data integration, reproducibility, and clinical translation.]]> Wed, 31 Dec 1969 19:00:00 EST Advanced deep learning strategies in nanopore RNA sequencing. Ling C, Lebeau B, Keong KC, Fullwood M
RNA Biol (Dec 2026)

The epitranscriptome comprises chemical modifications found on RNA molecules that play essential roles in co- and post-transcriptional gene regulation. Dysregulation of these modifications has been implicated in various diseases, fuelling interest in evaluating them as emerging biomarkers and therapeutic targets. Nanopore direct RNA sequencing provides a powerful platform for profiling diverse RNA modifications at single-molecule resolution, but the complexity of the signals requires advanced computational approaches for interpretation. Artificial intelligence, particularly deep learning (DL), has become central to this effort. While classical DL architectures such as convolutional and recurrent neural networks have been widely applied, more recent approaches employ specialized learning frameworks and ensemble strategies to address challenges of data scarcity, noise, and biological variability while providing higher resolution output. In this review, we summarize these developments and highlight future multidisciplinary opportunities at the intersection of artificial intelligence and biology for characterizing the epitranscriptome obtained with direct RNA nanopore sequencing.]]> Wed, 31 Dec 1969 19:00:00 EST TiSMeD: A tissue-specific methylation and expression database for biomarker and translational applications. Cheng J, Lin Z, Wu L, Li Q, Yin H, Wang H, Chen H, Chen X, Ji ZL
Mol Ther Nucleic Acids (Jun 2026)

Tissue-specific methylation sites (TSMs) are important epigenetic features associated with gene regulation, tissue development, and disease pathogenesis. However, the lack of comprehensive and reliable resources for TSMs restricts advancements in epigenetic and translational research. We present TiSMeD (http://www.bio-add.org/TiSMeD/), a multi-omics database integrating 6,782 DNA methylation, 16,894 transcriptome, and 241 proteome profiles across 48 normal human tissues. Using a scoring framework based on SPM and Tscore, we identified 67,427 high-confidence TSMs, 4,607 tissue-specific genes, and 2,833 tissue-specific proteins, along with over 11 million housekeeping methylation sites. TiSMeD enables interactive exploration and data retrieval, supporting biomarker discovery and disease research. We demonstrate its utility in tracing the tissue-of-origin of cell-free DNA (cfDNA), prioritizing 1,849 cancer biomarkers from The Cancer Genome Atlas (TCGA), and constructing a multi-cancer tracing and diagnostic model achieving 95.7% accuracy. TiSMeD serves as a robust, user-friendly platform integrating multi-omics data to advance epigenetic research and biomarker translation.]]> Wed, 31 Dec 1969 19:00:00 EST Melatonin-enabled omics: understanding plant responses to single and combined abiotic stresses for climate-smart agriculture. Raza A, Li Y, Charagh S, Guo C, Zhao M, Hu Z
GM Crops Food (Dec 2026)

Climate change-driven single and combined abiotic stresses pose escalating threats to sustainable, climate-smart agriculture and global food security. Melatonin (MLT, a powerful plant biostimulant) has established noteworthy potential in improving stress tolerance by regulating diverse physiological, biochemical, and molecular responses. Therefore, this review delivers a comprehensive synopsis of MLT-enabled omics responses across genomics, transcriptomics, proteomics, metabolomics, miRNAomics, epigenomics, phenomics, ionomics, and microbiomics levels that collectively regulate plant adaptation to multiple abiotic stresses. We also highlight the crosstalk between these omics layers and the power of integrated multi-omics (panomics) approaches to harness the complex regulatory networks underlying MLT-enabled stress tolerance. Lastly, we argue for translating these omics insights into actionable strategies through advanced genetic engineering and synthetic biology platforms to develop MLT-enabled, stress-smart crop plants.]]> Wed, 31 Dec 1969 19:00:00 EST Parthenogenote-derived brain unveils the critical role of paternal genome in neural development. Takechi M, Zhu Y, Lu Z, Zeng Y, Mizutani KI, Nakano T, Shen L, Yamaguchi S
Sci Rep (Jun 2026)

Genomic imprinting, an epigenetic mechanism that governs parent-of-origin-specific gene expression, is essential for mammalian development, yet its role in late-stage development remains unclear due to the lethality of parthenogenetic (Pg) embryos. Here, we establish cell replacement with parthenogenote-derived cells (CReP), a blastocyst complementation strategy that enables survival and tissue-specific contribution of Pg-derived cells. By creating tissue-specific niches in recipient embryos, CReP allows targeted incorporation of Pg-derived cells into late-stage tissues. Brain-targeted CReP showed that Pg-derived cells can participate in neural development but exhibit impaired maintenance of neuronal-glial balance, accompanied by increased Notch signaling and reduced expression of the paternally expressed gene Dlk1. Recombinant Dlk1 attenuated Notch activity and shifted neuronal differentiation toward control levels. These findings support a key contribution of the paternal genome to neural stem cell expansion and balanced cell fate decisions, in part through Dlk1-Notch-related pathways. The CReP model provides a powerful platform for investigating genomic imprinting and parental genome contributions in development and disease.]]> Wed, 31 Dec 1969 19:00:00 EST A cell type enrichment analysis tool for brain DNA methylation data (CEAM). Müller J, Laroche VT, Imm J, Weymouth L, Harvey J, Reijnders RA, Smith AR, van den Hove D, Lunnon K, Cavill R, Pishva E
Epigenetics (Dec 2026)

DNA methylation (DNAm) signatures are highly cell type-specific, yet most epigenome-wide association studies (EWAS) are performed on bulk tissue, potentially obscuring critical cell type-specific patterns. Existing computational tools for detecting cell type-specific DNAm changes are often limited by the accuracy of cell type deconvolution algorithms. Here, we introduce CEAM (Cell-type Enrichment Analysis for Methylation), a robust and interpretable framework for cell type enrichment analysis in DNA methylation data. CEAM applies over-representation analysis with cell type-specific CpG panels from Illumina EPIC arrays derived from nuclei-sorted cortical post-mortem brains from neurologically healthy aged individuals. The constructed CpG panels were systematically evaluated using both simulated datasets and published EWAS results from Alzheimer's disease, Lewy body disease, and multiple sclerosis. CEAM demonstrated resilience to shifts in cell type composition, a common confounder in EWAS, and remained robust across a wide range of differentially methylated positions, when upstream modeling of cell type composition was modeled with sufficient accuracy. Application to existing EWAS findings generated in neurodegenerative diseases revealed enrichment patterns concordant with established disease biology, confirming CEAM's biological relevance. The workflow is publicly available as an interactive Shiny app (https://um-dementia-systems-biology.shinyapps.io/CEAM/) enabling rapid, interpretable analysis of cell type-specific DNAm changes from bulk EWAS.]]> Wed, 31 Dec 1969 19:00:00 EST Global analyses of genomic and epigenomic influences on gene expression reveal as a major regulator of cardiac gene expression in response to catecholamine challenge during heart failure. Lahue C, Ravindran S, Dalal A, Avetisyan R, Rau CD
Epigenetics (Dec 2026)

Heart failure arises from maladaptive remodelling driven by genetic and epigenetic networks. Using a systems genetics framework, we mapped how DNA variants and CpG methylation shape cardiac transcriptomes during beta adrenergic stress in the Hybrid Mouse Diversity Panel, a cohort of over 100 fully inbred mouse strains. Expression QTLs (eQTLs), methylation QTLs (mQTLs) and methylation-driven eQTLs (emQTLs) were generated from over 13k expressed genes and 200k hypervariable CpGs in left ventricles. We discovered hundreds of regulatory 'hotspots' that control large portions of the genome, including several that regulate over 10% of the transcriptome and/or methylome. Approximately 16% of these hotspots overlapped with prior GWAS or EWAS signals. We focus on a hotspot on chromosome 12 and identify the serpine peptidase inhibitor , as the most likely driver gene in this hotspot. Experimental knockdown of in neonatal rat ventricular cardiomyocytes blunted hypertrophy induced by a variety of hypertrophic signals, while altering predicted target expression and modulating the activity of and . Together, these findings position as a major regulator of stress-responsive cardiac gene programs, highlighting how integration of genetic and epigenetic signals can pinpoint key drivers of heart failure.]]> Wed, 31 Dec 1969 19:00:00 EST Neuronutrition in ASD: Involvement of gut microbiota, oxidative stress and inflammatory markers. Avolio E, Olivito I, Minervini D, Soda T, De Bartolo A, Rocca C, Alò R, Facciolo RM
Neurosci Biobehav Rev (Aug 2026)

Autism spectrum disorder (ASD) is a neurodevelopmental disorder displaying altered human behaviors, such as social interaction impairments, stereotypical/repetitive activities and emotional dysregulation. Children with ASD are often affected by gastrointestinal problems and gut microbiota dysbiosis. Inflammation and immune dysfunction are key contributors to ASD, as shown by high proinflammatory cytokines and oxidative stress. Indeed, notable implication of the nuclear factor kappa B in the severity of ASD derives from its ability to amplify neuroinflammation. This narrative review focused attention on neuronutrition and gut microbiota manipulation for mitigation of ASD symptoms, including neuroinflammation and oxidative stress. Studies in both rodents and humans with ASD have revealed that both pure and mixed Lactobacillus and Bifidobacterium were effective in ameliorating behavioral symptoms and GABA/glutamate imbalance. Often, the combined use of probiotics and prebiotics can have greater health benefits in ASD. Additionally, dietary interventions and microbiota transfer therapies along with low-to-moderate-intensity exercise have been proposed to improve gastrointestinal and behavioral symptoms. However, despite some encouraging results, biases in the neuronutrition/microbiota literature still exist. Indeed, many studies rely on small sample sizes, cross-sectional designs, and heterogeneous populations that differ in diet, medications, and comorbidities. In this context, the development of a precision diet tailored to individual gut microbiome profiles will allow for a broader understanding of the microbial ecosystem and relative therapeutical applications. Hence, by integrating metagenomics, metabolomics, epigenomics, with evaluation of environmental and nutritional factors, it will be possible to significantly improve the quality of life for people with ASD and their families.]]> Wed, 31 Dec 1969 19:00:00 EST Mass Spectrometry-Based Proteomics for Assessing Epitranscriptomic Regulations. Yang YY, Cao Z, Wang Y
Mass Spectrom Rev (2026)

Epitranscriptomics is a rapidly evolving field that explores chemical modifications in RNA and how they contribute to dynamic and reversible regulations of gene expression. These modifications, for example, N-methyladenosine (mA), are crucial in various RNA metabolic processes, including splicing, stability, subcellular localization, and translation efficiency of mRNAs. Mass spectrometry-based proteomics has become an indispensable tool in unraveling the complexities of epitranscriptomics, offering high-throughput, precise protein identification, and accurate quantification of differential protein expression. Over the past two decades, advances in mass spectrometry, including the improvement of high-resolution mass spectrometers and innovative sample preparation methods, have allowed researchers to perform in-depth analyses of epitranscriptomic regulations. This review focuses on the applications of bottom-up proteomics in the field of epitranscriptomics, particularly in identifying and quantifying epitranscriptomic reader, writer, and eraser (RWE) proteins and in characterizing their functions, posttranslational modifications, and interactions with other proteins. Together, by leveraging modern proteomics, researchers can gain deep insights into the intricate regulatory networks of RNA modifications, advancing fundamental biology, and fostering potential therapeutic applications.]]> Wed, 31 Dec 1969 19:00:00 EST Paternal fenvalerate exposure causes autism-like behavior partly by altering epigenetic reprogramming of the imprinted gene IGF2 in fetal brain and paternal sperm. Qi XM, Shao J, Zhu QL, Deng ZY, Wang T, Chen HR, Xu LH, Li JJ, Wang M, Xu DX, Wang B, Meng XH
Ecotoxicol Environ Saf (Jul 2026)

Fenvalerate, a representative type II pyrethroid insecticide, is well established in the literature. Fenvalerate exerts developmental and neurological toxicity. We assessed whether paternal fenvalerate exposure induces autism-like behavioral alterations in offspring using a mouse model. Behavioral tests, including the three-chamber social interaction, self-grooming, and marble-burying tests, showed altered social and repetitive behaviors in offspring from fenvalerate-exposed fathers. NeuN, a mature neuronal marker, was reduced in the medial prefrontal cortex (mPFC) of weaning offspring from paternal fenvalerate-exposed groups. Nissl staining showed that the number of surviving neurons is reduced in the mPFC of weaning pups with paternal exposure to fenvalerate. Nestin, a marker for neural stem cells, was decreased in the fetal forebrain from paternal fenvalerate-exposed groups. Transcriptome analysis and RT-PCR showed that insulin-like growth factor 2 (IGF2), a neurotrophic factor, was downregulated in the paternal fenvalerate-exposed group. IGF2 protein was reduced in the fetal forebrain from paternal fenvalerate-exposed group. In addition, paternal fenvalerate exposure reduced methylation of the IGF2 imprinted control region (ICR) in fetal forebrain and paternal sperm. In conclusion, autism-like behaviors appear in offspring after paternal exposure to fenvalerate, which may partly be related to disruptions in epigenetic reprogramming of IGF2 in the developing brain and paternal sperm.]]> Wed, 31 Dec 1969 19:00:00 EST Disease-Associated Remodeling of m6A RNA Methylation in Human Interstitial Cells From Fibro-Calcific Aortic Valves. Valerio V, Molla O, Massaiu I, Garoffolo G, Myasoedova VA, Chiesa M, Poggio P
FASEB J (Jun 2026)

Calcific aortic valve disease is common in older adults and a major cause of aortic stenosis. Despite its clinical impact, there are still no effective drugs that slow disease progression, and treatment largely relies on surgical or transcatheter valve replacement once stenosis becomes severe and symptomatic. Beyond established roles for inflammation and tissue remodeling, recent evidence suggests that chemical modifications of RNA may influence how valve cells shift toward fibro-calcific states. In this study, we compared human valvular interstitial cells isolated from non-calcified valves and from fibro-calcific stenotic valves, profiling RNA modifications using direct RNA sequencing. The resulting epitranscriptomic patterns clearly separated control from diseased cells and revealed an overall increase in detected modification sites in disease, alongside site-specific gains and losses across selected transcripts. Network-based prioritization highlighted genes linked to extracellular matrix remodeling and inflammatory signaling, pointing to stress-responsive regulators as notable candidates. Overall, these findings support the idea that disease-associated RNA modification remodeling accompanies, and may help shape, key cellular programs in calcific valve disease, providing a focused set of targets for future functional validation and potential non-surgical therapeutic exploration.]]> Wed, 31 Dec 1969 19:00:00 EST Epigenetic research methods and animal models for intervertebral disc degeneration (Review). Cui X, Zeng L, Zhang W, Xi L, Wang R, Jia D, Safa , Feng H, Jia H
Mol Med Rep (Jul 2026)

Intervertebral disc degeneration (IVDD) is increasingly recognized as a systemic collapse of the epigenetic regulatory network, driven by cellular senescence and environmental stressors. The present review provides an overview of the epigenetic regulatory mechanisms governing IVDD, focusing on the dynamic interplay between DNA methylation, histone modifications, N6‑methyladenosine RNA methylation and the non‑coding RNA regulatory triad (microRNAs, long non‑coding RNAs and circular RNAs). The present study evaluates advanced research methodologies (ranging from site‑specific methylation typing and transposase accessible chromatin sequencing to single‑cell multi‑omics and artificial intelligence‑driven predictive modeling) that resolve the spatial and cellular heterogeneities of the degenerating disc niche. Furthermore, the translational constraints of current animal models were critically assessed, advocating for a strategic shift from acute needle‑puncture insults to physiologically relevant aging and genetically engineered progeroid models to better recapitulate human 'epigenetic drift'. Finally, the therapeutic potential of targeted epigenetic editing via CRISPR/dCas9 systems and the development of stimuli‑responsive nanocarriers for precision delivery are highlighted. By bridging methodological innovation with robust model selection, the present review offers a roadmap for transitioning molecular insights into clinical regenerative therapies for spinal health.]]> Wed, 31 Dec 1969 19:00:00 EST Interplay of Genetic and Biomarker Signatures in Oxidative Stress and Inflammation: Advancing Parkinson's Disease Research Through Emerging Omics Technologies. Vig H, Mishra A, Wal A
Curr Neurovasc Res (Jun 2026)

Parkinson's disease (PD) is a progressive neurodegenerative illness characterized by loss of dopaminergic neurons and misfolded α-synuclein aggregation. The pathophysiology of PD involves the interplay of oxidative stress, neuroinflammation, and genetic variables. This review provides an overview of the ways oxidative stress and neuroinflammation interact with genetic and epigenetic pathways in PD, as well as how omics technologies have aided in the identification of biomarkers that can be targeted by treatments.]]> Wed, 31 Dec 1969 19:00:00 EST Cholangiocyte biology in primary sclerosing cholangitis and other cholangiopathies: pathogenesis, clinical insights, and experimental tools. Jalan-Sakrikar N, Anwar AA, Ali A, Nasser-Ghodsi N, Felzen A, Huebert RC, LaRusso NF, O'Hara SP
Physiol Rev (Jul 2026)

Cholangiocytes are specialized epithelial cells that line the intrahepatic and extrahepatic biliary tree and play a critical role in bile modification, liver homeostasis, and response to injury. Cholangiocytes exhibit notable heterogeneity and plasticity, and their dysfunction is central to a spectrum of diseases targeting the bile ducts, collectively called cholangiopathies. These disorders include genetic, infectious, immune-mediated, and malignant diseases, with primary sclerosing cholangitis (PSC) representing one of the most complex and enigmatic of these disorders. PSC is a progressive, fibro-inflammatory disease of the bile ducts that is closely linked to inflammatory bowel disease, carries a heightened risk of cancer, and lacks any approved therapies. This review explores the biology of cholangiocytes, including their development, functional plasticity, and roles in secretion, absorption, and cellular signaling. We provide a detailed examination of cholangiopathies, particularly PSC, a complex cholangiopathy characterized by a paradoxical state of cholangiocyte senescence and hyperproliferation. We describe how immune cell dysfunction, the gut microbiome, genetic predispositions, and environmental factors converge to mediate PSC pathogenesis. We revisit the foundational technologies that empowered early discoveries and shaped the field as we know it today. We also explore how newer techniques such as organoid cultures, single-cell transcriptomics, epigenomics, and spatialomics have transformed our modern understanding of biliary pathophysiology. Finally, we provide an overview of existing rodent models of cholangiopathies and discuss their relevance to human disease. PSC remains therapeutically unaddressed, and thus ongoing multidisciplinary efforts are essential to developing targeted interventions. This review serves as a comprehensive resource for researchers and clinicians navigating the rapidly evolving landscape of cholangiocyte-centered liver disease research.]]> Wed, 31 Dec 1969 19:00:00 EST [Role and limitations of genome-wide DNA methylation profiling in the diagnosis of brain tumors]. Teng LH, Lu DH
Zhonghua Bing Li Xue Za Zhi (Jun 2026)

Genome-wide DNA methylation profiling, a high-throughput epigenomic technology, systematically examines the methylation status of CpG sites across the genome to generate "methylation fingerprints" that reflect cellular origins and developmental states. This technique has emerged as a transformative tool in the diagnosis of central nervous system (CNS) tumors. This article introduces the principles of this technology, along with its significant applications and major limitations in the diagnosis of CNS tumors. It proposes that current pathological diagnosis of CNS tumors should adopt an integrated diagnostic model centered on the pathologist, emphasizing that methylation profiling serves as an adjunctive tool rather than a replacement. Any methylation-derived result must be interpreted within the comprehensive context of clinical, radiological, histopathological, and molecular data. In the future, with advances in explainable artificial intelligence, multi-omics integration, and international standardization efforts, this technology is expected to evolve from a "revolutionary tool" into an "intelligent assistant" deeply integrated with pathological diagnosis.]]> Wed, 31 Dec 1969 19:00:00 EST Beyond Weight: Systems Biology and Precision Medicine Redefine Obesity as a Multidimensional Disease. Liu Y, Yang Y, Zhu L, Peng W
Diabetes Obes Metab (Jul 2026)

Traditional weight-centered models do not fully capture the biological complexity of obesity. Systems biology offers a new framework by integrating molecular, cellular, clinical, and environmental information to reframe obesity as a heterogeneous, multidimensional disease.]]> Wed, 31 Dec 1969 19:00:00 EST Charting the human-specific properties of gene expression networks in the infant prefrontal cortex. Klavert J, Radjabzadeh D, Gonzalez Sanchez E, Castelijns B, Timpanaro IS, Boers J, Fabro F, Vroeg In de Wei G, Bindels E, Kondova I, Gribnau J, Creyghton MP
Sci Adv (Jun 2026)

Human infancy is characterized by protracted brain development coinciding with sensitive periods of extensive synaptic remodeling. Whether this is supported by human infant-specific transcriptional programs is unknown as comparative material in closely related primate species was unavailable. Here, we analyze rare newborn chimpanzee and age-matched human and rhesus macaque brain samples using single-cell transcriptomics and epigenomics. We identify a human infant-specific transcriptional program in immature oligodendrocytes that is overrepresented in autism risk genes and patient gene expression changes. Furthermore, a human infant-specific transcriptional program in the neural lineage is overrepresented in Parkinson's disease risk genes and patient gene expression changes. Both of these programs are part of a core transcriptional network that contains human-specific sequence changes in regulatory DNA and lacks cell lineage specificity. Our study provides insights into the stage-specific properties of human evolution during early infancy and sheds light on the human-specific propensities to neural disease.]]> Wed, 31 Dec 1969 19:00:00 EST