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Nong, Y.

Publications and source records attributed to Nong, Y..

7 recordsLinked to original sources

Long-term Locus Coeruleus Stimulation Exacerbates Tau Pathology in PS19 Mice

BackgroundAlzheimers disease (AD) is the most common form of dementia, characterized by the accumulation of amyloid-{beta} (A{beta}) plaques and hyperphosphorylated Tau tangles. The locus coeruleus (LC) is among the first brain regions to show degeneration and Tau pathology during the early stages of AD. Previous studies have demonstrated that short-term chemogenetic LC stimulation can improve memory performance in the TgF344-AD rat model, while long-term norepinephrine (NE) reuptake inhibition can worsen memory deficits in the ADLPTau mouse model. However, the effects of long-term LC stimulation in Tau mouse models on memory, synaptic plasticity, and tauopathy remain unclear. ObjectiveTo evaluate the impact of long-term locus coeruleus stimulation on memory, synaptic plasticity, and tauopathy in PS19 mice using behavioral paradigms, electrophysiological recordings, and immunohistochemical analysis. MethodsThe radial arm water maze and fear conditioning test were conducted to assess memory performance in PS19 mice with and without long-term LC stimulation. Hippocampal long-term potentiation was recorded to evaluate the effect of long-term LC stimulation on synaptic plasticity. Immunohistochemistry was employed to examine Tau phosphorylation, neurodegeneration, and neuroinflammation. ResultsLong-term LC stimulation in PS19 mice exacerbated spatial memory deficits in the water maze, impaired contextual fear memory, reduced hippocampal LTP, and increased AEP expression, Tau hyperphosphorylation, and astrocyte activation. ConclusionLong-term LC stimulation may exacerbate memory deficits in PS19 mice by impairing synaptic plasticity and increasing neural degeneration in the hippocampus. Elevated norepinephrine levels resulting from long-term LC stimulation may increase AEP expression, contributing to Tau hyperphosphorylation in the LC.

pathology↗

Carnosinylation of Cardiac Antigens Attenuates Immunogenic Responses and Improves Function in Failing Hearts

ObjectiveTo investigate the effects of carnosine on heart failure and to examine whether this is associated with reduced immunogenicity of oxidatively-generated aldehyde modified proteins. BackgroundHeart failure is associated with the accumulation of lipid derived aldehydes that form immunogenic protein adducts. However, the pathological impact of these aldehydes and aldehyde-modified proteins in heart failure has not been assessed. Histidyl dipeptides, such as carnosine found in the heart, bind to aldehydes, and their protein adducts. However, the effects of carnosine on heart failure or the antigenicity of aldehyde modified proteins have not been studied. MethodsMale, wild type C57BL/6J mice were subjected to either sham or transverse aortic constriction (TAC) surgery. To increase carnosine levels, they were placed on drinking water with or without {beta}-alanine prior to surgery, and for the remainder of the study. Cardiac function was evaluated by echocardiography, and the levels of histidyl dipeptides, immune cell populations, and CD4+ T cell activation were assessed via LC-MS/MS and flow cytometry, respectively. ResultsMyocardial levels of histidyl dipeptides decreased at both 3- and 8-weeks post-TAC. Supplementation with {beta}-alanine increased myocardial histidyl dipeptide levels, attenuated adverse cardiac remodeling, and reduced aldehyde stress. Carnosine formed covalent bond with protein-bound aldehydes in the failing heart, reducing their antigenic potential and decreasing activation of dendritic cells and CD4+ T cells in vitro. {beta}-alanine supplementation decreased the population of CD11b+CD64-Ly6G+ neutrophils and CD4+ CD44+ effector T cells in the failing heart. ConclusionsIncreasing myocardial carnosine levels reduces aldehyde stress, dampens maladaptive immune responses, and preserves cardiac function during heart failure. HIGHLIGHTSO_LILevels of endogenous dipeptide carnosine are depleted in failing hearts, while supplementation of the carnosine precurson {beta}-alanine increases myocardial carnosine and preserves cardiac function during heart failure. C_LIO_LIHeart failure is associated with increased activation and infiltration of CD4+ T cells and generation of aldehyde modified protein adducts in failing hearts. C_LIO_LIThe free aldehyde moiety of aldehyde modified protein adducts activates CD4+ T cells through dendritic cell presentation and capping this moiety with carnosine diminishes their antigencity. C_LIO_LIIncreasing myocardial carnosine levels diminishes aldehyde stress and activation of CD4+ T cells during heart failure. C_LI GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=199 SRC="FIGDIR/small/671840v2_ufig1.gif" ALT="Figure 1"> View larger version (42K): org.highwire.dtl.DTLVardef@28fc7corg.highwire.dtl.DTLVardef@d851ccorg.highwire.dtl.DTLVardef@1e24a5dorg.highwire.dtl.DTLVardef@18023b6_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

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↗

Phase synchrony between prefrontal noradrenergic and cholinergic signals indexes inhibitory control

Inhibitory control is a critical executive function that allows animals to suppress their impulsive behavior in order to achieve certain goals or avoid punishment. We investigated norepinephrine (NE) and acetylcholine (ACh) dynamics and population neuronal activity in the prefrontal cortex (PFC) during inhibitory control. Using fluorescent sensors to measure extracellular levels of NE and ACh, we simultaneously recorded prefrontal NE and ACh dynamics in mice performing inhibitory control tasks. The prefrontal NE and ACh signals exhibited strong coherence at 0.4-0.8 Hz. Although inhibition of locus coeruleus (LC) neurons projecting to the PFC impaired inhibitory control, inhibiting LC neurons projecting to the basal forebrain (BF) caused a more profound impairment, despite an approximately 30% overlap between LC neurons projecting to the PFC and BF, as revealed by our tracing studies. The inhibition of LC neurons projecting to the BF did not diminish the difference in prefrontal NE/ACh signals between successful and failed trials; instead, it abolished the difference in NE-ACh phase synchrony between successful and failed trials, indicating that NE-ACh phase synchrony is a task-relevant neuromodulatory feature. Chemogenetic inhibition of cholinergic neurons that project to the LC region did not impair inhibitory control, nor did it abolish the difference in NE-ACh phase synchrony between successful or failed trials, further confirming the relevance of NE-ACh phase synchrony to inhibitory control. To understand the possible effect of NE-ACh synchrony on prefrontal population activity, we employed Neuropixels to record from the PFC during inhibitory control. The inhibition of LC neurons projecting to the BF not only reduced the number of prefrontal neurons encoding inhibitory control, but also disrupted population firing patterns representing inhibitory control, as revealed by a demixed principal component (dPCA) analysis. Taken together, these findings suggest that the LC modulates inhibitory control through its collective effect with cholinergic systems on population activity in the prefrontal cortex. Our results further indicate that NE-ACh phase synchrony is a critical neuromodulatory feature with important implications for cognitive control.

neuroscience↗

PathoGD: an integrative genomics approach for CRISPR-based target design of rapid pathogen diagnostics

The design of highly specific primers and guide RNAs (gRNA) for CRISPR-based diagnostics is often a laborious process. Several tools exist for gRNA design, but most are tailored for genome editing applications. Here, we present PathoGD, an end-to-end bioinformatic pipeline comprising pangenome and k-mer modules for rapid and high-throughput design of primers and gRNAs for CRISPR-Cas12a-based pathogen detection. We validated and demonstrated high specificity of a subset of PathoGD-designed primers and gRNAs for the detection of Neisseria gonorrhoeae and Streptococcus pyogenes. PathoGD will serve as an important resource for designing CRISPR-based diagnostic assays for current and emerging pathogens.

bioinformatics↗

UBE3A and transsynaptic complex NRXN1-CBLN1-GluD1 in a hypothalamic VMHvl-arcuate feedback circuit regulates aggression

The circuit origins of aggression in autism spectrum disorder remain undefined. Here we report Tac1-expressing glutamatergic neurons in ventrolateral division of ventromedial hypothalamus (VMHvl) drive intermale aggression. Aggression is increased due to increases of Ube3a gene dosage in the VMHvl neurons when modeling autism due to maternal 15q11-13 triplication. Targeted deletion of increased Ube3a copies in VMHvl reverses the elevated aggression adult mice. VMHvl neurons form excitatory synapses onto hypothalamic arcuate nucleus AgRP/NPY neurons through a NRXN1-CBLN1-GluD1 transsynaptic complex and UBE3A impairs this synapse by decreasing Cbln1 gene expression. Exciting AgRP/NPY arcuate neurons leads to feedback inhibition of VMHvl neurons and inhibits aggression. Asymptomatic increases of UBE3A synergize with a heterozygous deficiency of presynaptic Nrxn1 or postsynaptic Grid1 (both ASD genes) to increase aggression. Targeted deletions of Grid1 in arcuate AgRP neurons impairs the VMHvl to AgRP/NPY neuron excitatory synapses while increasing aggression. Chemogenetic/optogenetic activation of arcuate AgRP/NPY neurons inhibits VMHvl neurons and represses aggression. These data reveal that multiple autism genes converge to regulate the VMHvl-arcuate AgRP/NPY glutamatergic synapse. The hypothalamic circuitry implicated by these data suggest impaired excitation of AgRP/NPY feedback inhibitory neurons may explain the increased aggression behavior found in genetic forms of autism. One Sentence SummaryA feedback circuit in the hypothalamus that inhibits aggression is impaired by converging autism genetic defects.

neuroscience↗

Echocardiography-guided percutaneous left ventricular intracavitary injection as a cell delivery approach in infarcted mice

BackgroundIn the field of cell therapy for heart disease, a new paradigm of repeated dosing of cells has recently emerged. However, the lack of a repeatable cell delivery method in preclinical studies in rodents is a major obstacle to investigating this paradigm. Methods and ResultsWe have established and standardized a method of echocardiography-guided percutaneous left ventricular intracavitary injection (echo-guided LV injection) as a cell delivery approach in infarcted mice. Here, we describe the method in detail and address several important issues regarding it. First, by integrating anatomical and echocardiographic considerations, we have established strategies to determine a safe anatomical window for injection in infarcted mice. Second, we summarize our experience with this method (734 injections). The overall survival rate was 91.4%. Previous studies results suggest that 1x106 cells delivered via this method yielded similar retention in the heart at 24 h as 1x105 cells delivered via intracoronary or intramyocardial injection. Lastly, we examined the efficacy of this cell delivery approach. Compared with vehicle treatment, cardiac mesenchymal cells (CMCs) delivered via this method improved cardiac function assessed both echocardiographically and hemodynamically. Furthermore, repeated injections of CMCs via this method yielded greater cardiac function improvement than single dose administration. ConclusionEcho-guided LV injection is a feasible, reproducible, relatively less invasive and effective delivery method for cell therapy in heart disease. It is an important approach that could move the field of cell therapy forward, especially with regard to repeated cell administrations.

physiology↗