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Kong, Y.

Publications and source records attributed to Kong, Y..

At least 37 records · Page 2Linked to original sources

Wearable Photonic Device for Multiple Biomarker Sampling and Detection Without Blood Draws

Blood draws or phlebotomy using needles have been practiced in clinics for several centuries and it often causes pain, discomfort, and inconvenience. Herein, we create a wearable photonic device by integrating a microlens array (MLA) and an optic microneedle array (OMNA) functionalized with immunobinding capacity for safe and needle-free biomarker sampling and detection. The MLA-integrated OMNA amplified and transmitted LED light at 595 nm into the skin through the OMNA, bypassing the light-absorbing melanin in the epidermal layer, and evenly distributing it in the capillary-enriched dermis. The 595 nm light was preferably absorbed by hemoglobin (Hb) and oxygen-Hb within the capillaries, triggering thermal dilation of capillaries without damaging them or causing petechiae. The light illumination resulted in remarkable increases in the concentrations of various blood biomarkers in the skin owing to capillary dilation and biomarker extravasation. These extravasated biomarkers bound specifically to the OMNA, which was covalently decorated with capture antibodies, each microneedle immobilized with one specific antibody. The multi-functional OMNA was extensively modified to amplify the immunobinding signals and achieve sensitivity superior to that of enzyme-linked immunosorbent assay (ELISA) kits. As a proof of concept, we validated the functionality of the prototype for minimally invasive sampling and precise multiplexed blood biomarker detection in two mouse models to quantify acute inflammation and specific antibody production. This cost-efficient device provides a promising platform for blood-free, multiplexed detection of blood biomarkers.

bioengineering↗

TOGGLE identifies fate and function process within a single type of mature cell through single-cell transcriptomics

Cells that appear transcriptionally identical can maintain vastly different functions or fates--an enduring blind spot in single-cell transcriptomics. Here we introduce TOGGLE, a self-supervised graph diffusion framework that delineates fine-grained functional heterogeneity within phenotypically stable cell populations. By combining deep diffusion learning with reinforcement-guided clustering and a BERT-inspired masking strategy, TOGGLE reconstructs hidden trajectories of cell fate without prior labels or temporal information. Applied across multiple single-cell RNA-seq datasets, TOGGLE achieves up to 90 % accuracy in unsupervised fate prediction, surpassing existing trajectory algorithms such as WOT and Cospar. It distinguishes ferroptotic, apoptotic, and intermediate neuronal states in ischemic stroke, with predictions experimentally validated in animal models. In neural stem cells TOGGLE reveals epigenetic memory of metabolic activity, linking local DNA demethylation and chromatin accessibility to mitochondrial RNA expression. We further introduce the Graph Diffusion Functional Map, which isolates subtle RNA functional groupings otherwise obscured by conventional dimensionality reduction. TOGGLE thus establishes a generalizable framework for mapping functional identity and epigenetic dynamics at single-cell resolution, providing new insights into cellular memory, regeneration, and disease mechanisms. Biographical NoteChens guidance comes from Dr. Alex P. Carll. Another mentor is Dr. Lu Cai, one of the contributors to the standardization of autophagy detection methods, whose research on criteria for identifying diabetes induced apoptosis has been included in numerous clinical guidelines. Professor Jinwen Ge is a State Council Special Allowance Expert of China. He has been involved in formulating medical standards for integrated traditional Chinese and Western medicine in China and has participated in developing retrieval/indexing norms for journals in the field of integrated traditional Chinese and Western medicine. Code and Data availabilityThe raw data for the hematopoiesis dataset can be accessed at the Gene Expression Omnibus database with accession number GSE140802, the reprogramming dataset with accession number GSE99915, the e-cigarette aerosol inhalation on mouse cardiac tissue with accession number GSE183614, the rat myocardial infarction dataset with accession number GSE253768, the ischemic stroke dataset with accession number GSE232429, and the adult NSC lineage dataset with accession number GSE209656 and GSE211786. All codes and guide page & analyzed data are full open available at: https://github.com/FullBlackWolf/TOGGLE?tab=readme-ov-file https://fullblackwolf.github.io/TOGGLE/ Key points(1) Previous studies have primarily focused on distinguishing cell types and different cellular subpopulations, whereas our tool is designed to identify subtle functional differences among highly similar cell states. For example, in Test2, it first isolates neurons undergoing cell death, then further differentiates early, intermediate, and late death stages, and separates ferroptosis from apoptosis as two major categories. Notably, ferroptosis and apoptosis share a large number of molecular pathways, making this task highly challenging. In addition, in Test4, our method discriminates fibroblasts with distinct immune-communication patterns, even though they do not show prominent separation or temporal progression on conventional UMAP plots. (2) We developed an innovative Graph Diffusion Functional Map that significantly reduces noise, resulting in clearer visualization of RNA functional groupings and enabling the detection of subtle functional differences in high-dimensional data. This provides a novel tool for pathway discovery. For instance, in Test4, we found that the KEGG inflammatory response pathway was most strongly activated in young mice, suggesting that e-cigarette exposure exerts more severe effects on immature cardiac tissue. (3) We implemented a novel trajectory-tracking strategy capable of distinguishing early, intermediate, and late stages of cellular programming, which we refer to as functional lineage tracing. In Test3, we successfully separated nearly indistinguishable aNSC and qNSC populations and further uncovered their methylation-regulated transcriptional programs, demonstrating that local DNA demethylation activates genes involved in cell proliferation and energy metabolism, thereby regulating the activation of quiescent neurons. (4) In the testing dataset, it was found that local DNA demethylation activates the expression of genes associated with cell proliferation and energy metabolism, thereby regulating the activation of quiescent neurons. Neuronal ferroptosis in ischemic stroke may be linked to the high expression of ferroptosis driver genes such as Ctsb, Mtdh, Ndrg1, Smad7, Cd82, and Acsl1.

bioinformatics↗

Electron-density informed effective and reliable de novo molecular design and lead optimization with ED2Mol

Generative drug design opens new avenues for discovering novel compounds within the vast chemical space rather than conventional screening against limited compound libraries. However, the practical utility of the generated molecules is frequently constrained, as many designs prioritize a narrow range of pharmacological properties while neglecting physical reliability, which hinders the success rate of subsequent wet-lab evaluations. To address this, we propose ED2Mol, a deep learning-based approach that leverages fundamental electron density information to improve de novo molecular generation and lead optimization. The extensive evaluations across multiple benchmarks demonstrate that ED2Mol surpasses existing methods in terms of generation success rate and >97% physical reliability. It also facilitates automated lead optimization that is not fully implemented by other methods using fragment-based strategies. Furthermore, ED2Mol exhibits generalizability to more challenging, unseen allosteric pocket benchmarks, attaining consistent performance in both de novo molecule generation and lead optimization. More importantly, ED2Mol has been applied to various real-world essential targets, successfully identifying wet-lab validated bioactive compounds, ranging from FGFR3 orthosteric inhibitors to CDC42 allosteric inhibitors and GCK allosteric activators. The directly generated binding modes of these compounds with target proteins are close to predictions through molecular docking and further validated via the X-ray co-crystal structure. All these results highlight ED2Mols potential as a useful tool in realistic drug design with enhanced effectiveness, physical reliability, and practical applicability.

bioinformatics↗

Cis-Regulatory Evolution of CCNB1IP1 Driving Gradual Increase of Cortical Size and Folding in primates

Neocortex expansion has a concerted relationship with folding, underlying evolution of human cognitive functions. However, molecular mechanisms underlying this significant evolutionary process remains unknown. Here, using tree shrew as an outgroup of primates, we identify a new regulator CCNB1IP1, which acquired its expression before the emergence of primates. Following the evolution of cis-regulatory elements, the CCNB1IP1 expression has steadily increased over the course of primate brain evolution, mirroring the gradual increase of neocortex. Mechanistically, we elucidated that CCNB1IP1 expression can cause an increase in neural progenitors through shortening G1 phase. Consistently, the CCNB1IP1 knock-in mouse model exhibited traits associated with enhanced learning and memory abilities. Together, our study reveals how changes in CCNB1IP1 expression may have contributed to the gradual evolution in primate brain.

evolutionary biology↗

Stage-Specific Transcriptome Landscape of Hepatocellular Carcinoma: Insights from Super and Poor Survivors with Prognostic Signature Identification

BackgroundThe prognosis for hepatocellular carcinoma (HCC) patients can vary significantly even within the same clinical stage. This study aims to characterize the stage-specific transcriptomic landscape of super survivors with HCC and identify a prognostic gene signature. MethodsWe analyzed data from The Cancer Genome Atlas (TCGA) for 76 matched super survivors (alive at 5 years) and poor survivors (deceased within 1 year) with HCC. Gene set enrichment analysis stratified by stage was conducted and a key prognostic gene signature was developed. The signature was then applied to the full TCGA cohort and independently validated in International Cancer Genome Consortium (ICGC) data. FindingsStage-specific transcriptomic profiling revealed distinct patterns in super survivors. Stage I and II showed positive enrichment in immune response pathways, while stage III exhibited enhanced catabolic activities and reduced glycolysis. Across all stages, cell cycle processes were less active in super survivors. A 19-gene signature, incorporating immune, metabolic, and cell cycle genes, accurately distinguished super from poor survivors with 91% accuracy (69/76). The signature reliably predicted overall survival in both the verification cohort (1-year, 3-year, and 5-year AUROCs of 0.82, 0.80, and 0.78) and the independent validation cohort (1-year and 3-year AUROCs of 0.80 and 0.83). Consistent AUROCs were observed across all tumor stages. InterpretationOur findings reveal a dynamic shift in HCC progression, with immune dominance in early stages and metabolic dominance in later stages, alongside reduced cell cycle activity across all stages. Integrating stage-specific transcriptomic profiles offers a promising approach to enhancing individualized management for HCC patients.

bioinformatics↗

Optogenetic stimulation of a cortical biohybrid implant guides goal directed behavior

Brain-computer interfaces (BCIs) hold exciting therapeutic potential, but tissue damage caused by probe insertion limits channel count. Biohybrid devices, in which the cell-device interface is crafted in the laboratory, hold promise to address this limitation, but these devices have lacked a demonstration of their applicability for BCI. We developed a biohybrid approach to engraft optogenetically-enabled neurons on the cortical surface housed in a 2D-scaffold of circular microwells. The engrafted neurons survived, exhibited spontaneous activity, and integrated with the host brain several weeks after implantation. We then trained mice with biohybrid implants to perform an optical stimulation task and showed that they could effectively report optogenetic stimulation of their neural graft. This demonstration shows that a cortical biohybrid implant can be used to transmit information to the brain of an implanted animal.

neuroscience↗

PTBP1 is upregulated by Zika virus infection via HIF-1alpha signal and hijacks NS1 protein to induce NS1 degradation to restrain viral replication

Zika virus (ZIKV), belonging to the Flaviviridae family, has been a severe threat to human health since the worldwide outbreak. ZIKV is capable of inducing fetal microcephaly, Guillain-Barre syndrome, and other serious neurological complications. Polypyrimidine tract-binding protein 1 (PTBP1) is a key member of the heterogeneous nuclear ribonucleoproteins (hnRNPs) family, functioning in selective mRNA splicing and gene expression regulation. Our previous study has indicated that the expression of PTBP1 increases in astrocytes upon ZIKV infection, yet the precise regulatory mechanisms underlying its role in viral replication remain elusive. In this study, we elucidated the specific pathway by which ZIKV upregulates PTBP1 expression through the activation of Hypoxia-inducible factor-1 (HIF-1) expression. Further investigation revealed that overexpression of PTBP1 effectively inhibits viral replication, whereas knockdown of PTBP1 significantly enhances viral replication. Mechanistically, using co-immunoprecipitation assays for protein interaction screening, we identified an interaction between PTBP1 and ZIKV non-structural protein NS1. Detailed studies demonstrated that PTBP1 bound and colocalized with NS1 to lead to the degradation of NS1 protein via a lysosomal pathway. Collectively, our findings unveil a novel mechanism underlying that ZIKV infection induces the expression of PTBP1 via the HIF-1 pathway, subsequently the accumulated PTBP1 binds to ZIKV NS1 protein to promote NS1 degradation, thereby effectively inhibiting viral replication. The study illustrates a distinct restricted cellular factor that regulates ZIKV replication, which provides a potential target for the control of the viral replication and pathogenesis during the ZIKV epidemic. ImportanceSince the outbreak of ZIKV infection among human in 2014, a Zika epidemic has caused Zika fever accompanied with fetal microcephaly, Guillain-Barre syndrome, and other neurological symptoms. Emerging evidence reveals that ZIKV infects astrocytes to specially induce the expression of polypyrimidine tract-binding protein 1 (PTBP1), one of hnRNPs members. However, the interplay between PTBP1 and ZIKV replication is highly concerned. Here, we uncover a distinct manner that ZIKV infection induces PTBP1 expression through the activation of hypoxia-inducible factor-1 (HIF-1) signal. Additionally, activation of HIF-1 signal hinders ZIKV replication relying on PTBP1 accumulation. Further investigations suggest that PTBP1 restrains ZIKV replication by interacting with ZIKV NS1 protein, thereby leading to the degradation of NS1 protein via a lysosomal pathway. Collectively, our findings illustrate a novel restricted cellular factor PTBP1 mediated by HIF-1 that regulates ZIKV replication, which provides a potential therapeutic target of the viral replication and pathogenesis against ZIKV pandemic.

microbiology↗

Critical assessment of nanopore sequencing for the detection of multiple forms of DNA modifications

While nanopore sequencing is increasingly used for mapping DNA modifications, it is important to recognize associated false-positive calls, as they can mislead biological interpretations. To assist biologists and methods developers, we describe a framework, modFDR, for rigorous evaluation that emphasizes the use of the false discovery rate with rationally designed negative controls capturing both general background and confounding modifications. Our critical assessment across multiple DNA modifications shows that while nanopore sequencing performs reliably for high-abundance modifications--including 5-methylcytosine (5mC) at CpG sites in mammalian cells and 5-hydroxymethylcytosine (5hmC) in mammalian brain cells--it produces a substantial fraction of false-positive detections for low-abundance modifications, such as 5mC at CpH sites, 5hmC, and N6-methyldeoxyadenine (6mA) in most mammalian cell types. Although newer models improve certain aspects, systematic false positives remain, and we further observe elevated false negatives for 5mCpG when benchmarked against orthogonal enzymatic methods. This study highlights the urgent need to incorporate modFDR into future methods development, evaluation, and biological studies, and advocates prioritizing nanopore sequencing for mapping abundant rather than rare modifications in biomedical applications.

genomics↗

DNA replication fork speed Acts as an Engine in Cortical Neurogenesis

DNA replication fork speed, which controls the rate of genome duplication, has emerged as a key regulator of cellular plasticity. However, its role in neurogenesis remains unexplored. Mini-chromosome maintenance complex (MCMs)-binding protein (MCMBP) functions as a chaperone for newly synthesized MCMs, increasing chromatin coverage to restrain fork speed. We demonstrate that selective deletion of MCMBP in neural progenitor radial glial cells (RGCs) accelerates fork speed, triggering widespread apoptosis, DNA damage, and micronuclei formation, ultimately activating p53 and causing microcephaly. Unexpectedly, concurrent deletion of Trp53 and Mcmbp further increased fork speed, leading to extensive RGC detachment from the ventricular zone and acquisition of outer-RGC characteristics. Mechanistically, we found that the MCM3 subunit coordinates DNA and centrosome duplication, thereby mediating RGC attachment. Behavioral analysis revealed that disruption of fork speed results in anxiety-like behavior in mice. These findings unveil a previously unrecognized role for replication fork speed in neurogenesis.

neuroscience↗

PEBP1 amplifies mitochondrial dysfunction induced integrated stress response

Mitochondrial dysfunction is involved in numerous diseases and the aging process. The integrated stress response (ISR) serves as a critical adaptation mechanism to a variety of stresses, including those originating from mitochondria. By utilizing thermal proteome profiling (TPP), we uncovered that phosphatidylethanolamine-binding protein 1 (PEBP1), also known as Raf kinase inhibitory protein (RKIP), is thermally stabilized by stresses which induce mitochondrial ISR. Depletion of PEBP1 impaired mitochondrial ISR activation by reducing eIF2 phosphorylation and subsequent ISR gene expression, which was independent of PEBP1s role in inhibiting the RAF/MEK/ERK pathway. Consistently, overexpression of PEBP1 potentiated ISR activation by heme-regulated inhibitor kinase (HRI), the principal eIF2 kinase in the mitochondrial ISR pathway. Real-time interaction analysis using luminescence complementation in live cells revealed an interaction between PEBP1 and eIF2, which was disrupted by eIF2 S51 phosphorylation. These findings suggest a role for PEBP1 in amplifying mitochondrial stress signals, thereby facilitating an effective cellular response to mitochondrial dysfunction. Therefore, PEBP1 may be a potential therapeutic target for diseases associated with mitochondrial dysfunction.

cell biology↗

Identification of Growth Differentiation Factor-15 as An Early Predictive Biomarker for Metabolic Dysfunction-Associated Steatohepatitis: A Nested Case-control Study of UK Biobank Proteomic Data

Background & AimsThe lack of non-invasive biomarkers for the early prediction of patients with metabolic dysfunction-associated steatohepatitis (MASH) is a major challenge for timely intervention. This study aims to determine the predictive capability for MASH long before its diagnosis by using six previously identified diagnostic biomarkers for metabolic dysfunction-associated steatotic liver disease (MASLD) with proteomic data from the UK Biobank. MethodsA nested case-control study comprising of a MASH group and three age- and sex-matched controls groups (metabolic dysfunction-associated steatosis, viral hepatitis, and normal liver controls) were conducted. Olink proteomics, anthropometric and biochemical data at baseline levels were obtained from the UK Biobank. The baseline levels of CDCP1, FABP4, FGF21, GDF15, IL-6 and THBS2 were analyzed prospectively to determine their predictive accuracy for subsequent diagnosis with a mean lag time of over 10 years. ResultsAt baseline, GDF15 demonstrated the best performance for predicting MASH occurrence at 5 and 10 years later, with an AUC of 0.90 at 5 years and 0.86 at 10 years. A predictive model based on four biomarkers (GDF15, FGF21, IL-6, and THBS2) showed AUCs of 0.88 at both 5 and 10 years. Furthermore, a protein-clinical model that included these four circulating protein biomarkers along with three clinical factors (BMI, ALT and TC) yielded AUCs of 0.92 at 5 years and 0.89 at 10 years. ConclusionGDF15 at baseline levels outperformed other individual circulating protein biomarkers for the early prediction of MASH. Our data suggest that GDF15 and the GDF15-based model may be used as easy-to-implement tools to identify patients with high risk of developing MASH at a mean lag time of over 10 years.

molecular biology↗

Dietary Bioactive Compounds Trigger Distinct Epigenetic and Metabolic Reprogramming in Lactobacillus acidophilus

Lactobacillus acidophilus ATCC 4356 (LA), a key probiotic in the human gut microbiota, offers several health benefits. While dietary bioactive compounds are known to influence gut microbiota, their specific mechanisms remain unclear. This study investigated how certain dietary bioactive compounds impact LA gene expression and metabolism. Results showed each compound produces unique transcriptional, metabolic, proteomic, and epigenetic profiles in LA. Notably, dietary compounds altered the epigenetic landscape through N4-methylcytosine (4mC) modification, a relatively underexplored form of methyl modification that may play a role in regulating gene transcription. For instance, genistein treatment up-regulated 76 genes and the down-regulated 130 genes in LA. A gene involved in mucus-binding proteins, crucial for bacterial adhesion, was up-regulated 38-fold, likely due to 4mC modifications. Additionally, the gene coding for the melibiose operon regulatory protein increased 78-fold, enhancing melibiose (a prebiotic) production with genistein, but only 1.1-fold with sodium butyrate. This study highlights the potential of dietary compounds for microbial metabolic engineering, offering a non-GMO method for modulating bacterial performance and other biotechnology applications. Graphical AbstractDietary compounds are able to modify the epigenetic landscape of Lactobacillus acidophilus ATCC 4356, resulting in significant transcriptomic, metabolic, and physiological changes. This approach differs from conventional genetic modification techniques for manipulating microbial strains. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=84 SRC="FIGDIR/small/608491v1_ufig1.gif" ALT="Figure 1"> View larger version (25K): org.highwire.dtl.DTLVardef@1d1f547org.highwire.dtl.DTLVardef@13e18a3org.highwire.dtl.DTLVardef@1c37e2dorg.highwire.dtl.DTLVardef@190be49_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

BMAP: a comprehensive and reproducible biomedical data analysis platform

In the realm of biomedical research, efficient data analysis and processing are crucial due to the escalating volume and complexity of data generated by research teams. Managing these vast arrays of localized data presents significant challenges, necessitating precise, efficient, and reproducible analysis methodologies to ensure the integrity and reliability of scientific outcomes. Traditional management of analysis codes, computing environments, and the inherent difficulties in result traceability due to team dynamics often lead to inefficiencies and potential risks in maintaining academic integrity. Furthermore, while online storage platforms such as Dryad, GitHub, and Docker facilitate data, code, and environment management, they do not inherently guarantee the reproducibility of results, with issues like data incompleteness, forgotten parameters, or software discrepancies posing additional challenges. To address these critical gaps, we developed a BioMedical data Analysis Platform (BMAP) to offer online and localized categorized management of research assets. BMAP enhances workflow efficiency by transforming complex pipelines into user-friendly web applications, promoting consistency and standardization across team analyses. Its comprehensive web analysis module and seamless integration with data and computing resources support automated result reproducibility and visualization. According to the assessment, 1,692 omics-related figures from 101 recent articles, across 45 visualization types, were tested with BMAP, which could cover 37.8% of the types and 64.3% of the figures. BMAP also enables the sharing and enhancement of research methods through its cloud platform, allowing researchers to utilize the previously developed and validated tools, thereby reducing redundant effort and minimizing analytical discrepancies due to methodological differences.

bioinformatics↗

Whole-genome DNA methylomes of Tree shrew brains reveal conserved and divergent roles of DNA methylation on sex chromosome regulation

The tree shrew (Tupaia belangeri) is a promising emerging model organism in biomedical studies, notably due to their evolutionary proximity to primates. To enhance our understanding of how DNA methylation is implicated in regulation of gene expression and the X chromosome inactivation (XCI) in tree shrew brains, here we present their first genome-wide, single-base-resolution methylomes integrated with transcriptomes from prefrontal cortices. We discovered both divergent and conserved features of tree shrew DNA methylation compared to that of other mammals. DNA methylation levels of promoter and gene body regions are negatively correlated with gene expression, consistent with patterns in other mammalian brains studied. Comparing DNA methylation patterns of the female and male X chromosomes, we observed a clear and significant global reduction (hypomethylation) of DNA methylation across the entire X chromosome in females. Our data suggests that the female X hypomethylation does not directly contribute to the gene silencing of the inactivated X chromosome nor does it significantly drive sex-specific gene expression of tree shrews. However, we identified a putative regulatory region in the 5 end of the X inactive specific transcript (Xist) gene, a key gene for XCI, whose pattern of differential DNA methylation strongly relate to its differential expression between male and female tree shrews. We show that differential methylation of this region is conserved across different species. Moreover, we provide evidence suggesting that the observed difference between human and tree shrew X-linked promoter methylation is associated with the difference in genomic CpG contents. Our study offers novel information on genomic DNA methylation of tree shrews, as well as insights into the evolution of X chromosome regulation in mammals.

genomics↗

A replicable and generalizable neuroimaging-based indicator of pain sensitivity across individuals

Developing neural indicators of pain sensitivity is crucial for revealing the neural basis of individual differences in pain and advancing individualized pain treatment. To identify reliable neural indicators of pain sensitivity, we leveraged six large and diverse functional magnetic resonance imaging (fMRI) datasets (total N=1046). We found replicable and generalizable correlations between nociceptive-evoked fMRI responses and pain sensitivity for laser heat, contact heat, and mechanical pains. These fMRI responses correlated more strongly with pain sensitivity than with tactile, auditory, and visual sensitivity. Moreover, we developed a machine learning model that accurately predicted not only pain sensitivity but also pain reduction from different interventions in healthy individuals. Notably, these findings were influenced considerably by sample sizes, requiring >200 for univariate correlation analysis and >150 for multivariate machine learning modelling. Altogether, we demonstrate the validity of decoding pain sensitivity from fMRI responses, thus facilitating interpretations of subjective pain reports and promoting more mechanistically informed investigation of pain physiology.

neuroscience↗

Hippocampal mGluR5 levels are comparable in Alzheimer's and control brains, and divergently influenced by amyloid and tau in control brain

BackgroundMetabotropic glutamate receptor 5 (mGluR5) modulates excitatory glutamatergic synaptic transmission and plays an important role in learning and memory formation and in neurodegeneration and amyloid deposition in Alzheimers disease (AD). Conflicting results on the cerebral mGluR5 levels in AD have been reported based on in vivo and postmortem studies. Here, we aimed to assess alterations in hippocampal mGluR5 expression in AD, and the associations between mGluR5 expression and pathologies. MethodsImmunofluorescence staining for mGluR5 was performed on postmortem brain tissue from 34 AD patients and 31 nondemented controls (NCs) and from aged 3xTg and arcA{beta} model mice of AD. Autoradiography was performed on brain tissue slices from arcA{beta} mice using mGluR5 tracer [18F]PSS232. Analysis of different cellular source of GRM5 RNA in human and mouse brains was performed. Proteomic profiling and pathway analysis were performed on hippocampal tissue from aged 3xTg mice and wild-type mice. ResultsNo differences in hippocampal mGluR5 expression or entorhinal cortical GRM5 RNA levels were detected between the AD and NC groups. Hippocampal mGluR5 levels increased with Braak stage and decreased with amyloid level in the NC group. No correlations were detected between the levels of mGluR5 and amyloid, tau, or Iba1/P2X7R in the hippocampus of AD patients and NC cases. Ex vivo autoradiography revealed comparable cerebral levels of [18F]PSS232 in arcA{beta} mice compared to nontransgenic mice. GO and KEGG pathway enrichment analyses revealed that the Shank3, Grm5 and glutamatergic pathways were upregulated in hippocampal tissue from aged 3xTg mice compared to wild-type mice. ConclusionThis study revealed no difference in hippocampal mGluR5 levels between AD patients and NCs and revealed the divergent influence of amyloid and tau pathologies on hippocampal mGluR5 levels in NCs. Species differences were observed in the GRM5 RNA level as well as at the cellular location. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=141 SRC="FIGDIR/small/595868v1_ufig1.gif" ALT="Figure 1"> View larger version (45K): org.highwire.dtl.DTLVardef@17c69aorg.highwire.dtl.DTLVardef@efbaf9org.highwire.dtl.DTLVardef@dc3c2corg.highwire.dtl.DTLVardef@f27038_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

Neuropeptide Y co-opts neuronal ensembles for memory lability and stability

Memory engrams are formed by activity-dependent recruitment of distinct subsets of excitatory principal neurons (or neuronal ensembles) whereas inhibitory neurons pivot memory lability and stability1-5. However, the molecular logic for memory engrams to preferentially recruit specific type of interneurons over other subtypes remains enigmatic. Using activity-dependent single-cell transcriptomic profiling6-8 in mice with training of cued fear memory and extinction, we discovered that neuropeptide Y (NPY)-expressing (NPY+) GABAergic interneurons in the ventral hippocampal CA1 (vCA1) region exert fast GABAergic inhibition to facilitate the acquisition of memory, but bifurcate NPY-mediated slow peptidergic inhibition onto distinct sub-ensembles underlying the extinction of single memory trace. Genetically encoded calcium and NPY sensors revealed that both calcium dynamics of NPY+ neurons and their NPY release in vCA1 ramp up as extinction learning progresses while behavioral state switches from "fear-on" to "fear-off". Bidirectional manipulations of NPY+ neurons or NPY itself demonstrated NPY is both necessary and sufficient to control the rate and degree of memory extinction by acting on two physically non-overlapping sub-ensembles composed of NPY1R- and NPY2R-expressing neurons. CRISPR/Cas9-mediated knockout of NPY2R or NPY1R further unravels that NPY co-opts its actions on these two sub-ensembles to gate early fast and late slow stages of extinction. These findings exemplify the intricate spatiotemporal orchestration of slow peptidergic inhibitions from single subtype of GABAergic interneurons to fine-tune engram lability verse stability of memory.

neuroscience↗

Human BioMolecular Atlas Program (HuBMAP): 3D Human Reference Atlas Construction and Usage

The Human BioMolecular Atlas Program (HuBMAP) aims to construct a reference 3D structural, cellular, and molecular atlas of the healthy adult human body. The HuBMAP Data Portal (https://portal.hubmapconsortium.org) serves experimental datasets and supports data processing, search, filtering, and visualization. The Human Reference Atlas (HRA) Portal (https://humanatlas.io) provides open access to atlas data, code, procedures, and instructional materials. Experts from more than 20 consortia are collaborating to construct the HRAs Common Coordinate Framework (CCF), knowledge graphs, and tools that describe the multiscale structure of the human body (from organs and tissues down to cells, genes, and biomarkers) and to use the HRA to understand changes that occur at each of these levels with aging, disease, and other perturbations. The 6th release of the HRA v2.0 covers 36 organs with 4,499 unique anatomical structures, 1,195 cell types, and 2,089 biomarkers (e.g., genes, proteins, lipids) linked to ontologies and 2D/3D reference objects. New experimental data can be mapped into the HRA using (1) three cell type annotation tools (e.g., Azimuth) or (2) validated antibody panels (OMAPs), or (3) by registering tissue data spatially. This paper describes the HRA user stories, terminology, data formats, ontology validation, unified analysis workflows, user interfaces, instructional materials, application programming interface (APIs), flexible hybrid cloud infrastructure, and previews atlas usage applications.

bioinformatics↗