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Wu, H.

Publications and source records attributed to Wu, H..

At least 163 records · Page 9Linked to original sources

Biomimetic Neoadjuvant Platform: Controlled Nanotoxicology as a Novel Approach to Preoperative Immunomodulation

The persistent immunosuppression and spatial heterogeneity of advanced solid tumors necessitate next-generation neoadjuvant platforms capable of reprogramming tumor microenvironments while overcoming resistance to immune checkpoint blockade. Addressing this unmet clinical challenge, we report a {beta}-glucan-empowered nano-neoadjuvant agents (NNAs) engineered through topology-guided supramolecular assembly of pathogen-mimetic {beta}-glucan motifs onto photoresponsive single-wall carbon nanotubes. This biomimetic architecture capitalizes on three synergistic mechanisms: (1) Dectin-1-mediated pathogen-associated molecular pattern recognition to rewire myeloid cell functionality, (2) endogenous leukocyte-hitchhiking delivery paradigm, and (3) spatiotemporally controlled photothermal ablation via near-infrared transducing SWNT cores. NNAs also orchestrates a proinflammatory cascade involving IL-12-dependent Th1 polarization and activation, effectively converting "cold" tumors into immunogenic niches. This strategy redefines preoperative therapeutic paradigms, offering a multimodal platform to harness the proinflammatory adjuvant effect of SWNTs for preoperative immunomodulation in advanced-stage malignancies. By bridging innate immune recognition with nanotechnology-enabled precision, this paradigm establishes a new roadmap for preoperative conditioning of advanced malignancies, offering a theranostic framework to transform surgical outcomes through immunologically informed nanomedicine design.

bioengineering↗

Obesity Increases Atherosclerosis Susceptibility via Inter-tissue miR-30e-SLC7A11 Axis

BackgroundWith obesity as a risk factor for atherosclerotic disease, recent research suggests that adipose tissue in obese animal models and humans can generate endocrine-like molecules that affect arterial health later on. Previous studies showed that microRNA-30e (miR-30e) level is elevated in atherosclerosis and solute carrier family 7 member 11 (SLC7A11), a cystine/glutamate transporter, is involved in atherogenesis. However, whether an endocrine-like link between the adipose-derived miR-30e-5p and SLC7A11 in the vascular endothelium can lead to obesity-caused atherosclerosis is unknown. MethodsMiRNA data mining and RT-PCR validations were used to demonstrate the positive association among serum level of miR-30e-5p, obesity, and coronary arterial disease in human patients. Transcriptomics (RNA-seq and single-nucleus RNA-seq), metabolomics, and in silico analysis were used to establish a miR-30e-5p-SLC7A11 regulation of central carbon metabolism, mitochondrial and endothelial cell (EC) function. Mouse models with EC-specific Slc7a11 knockout (EC-Slc7a11-/-) and gain or loss of function of miR-30e-5p were used to elucidate the detrimental role of this endocrine-like axis in obesity-related atherosclerosis. ResultsThe level of adipocyte-derived miR-30e-5p was significantly upregulated in obese humans with coronary artery disease and obese and atherosclerotic mice. Via serum exosomes, the adipocyte-generated miR-30e-5p targeted SLC7A11 mRNA in vascular ECs. SLC7A11 deficiency due to miR-30e-5p targeting dysregulated glutamate/cystine metabolism increased glycolysis, reduced oxidative phosphorylation, and impaired mitochondrial function. The EC dysfunction could be rectified by SLC7A11 overexpression or miR-30e-5p antagonism. Exogenously delivered miR-30e-5p phenocopied the increased atherosclerosis in EC-Slc7a11-/- mice. In contrast, miR-30e-5p antagomir treatment reduced atherosclerosis in Apoe-/- and ob/ob mice. ConclusionOur multi-omics approaches demonstrates that the adipose-derived miR-30e-5p downregulated SLC7A11 mRNA in ECs via tissue crosstalk. The resulting EC dysfunction led to obesity-related atherosclerosis in mice. These findings underscore a causality between obesity and atherosclerosis in the context of cardiovascular-kidney-metabolic syndrome.

molecular biology↗

Supramolecular Biomimetic Topology: Macrophage-Engaged Neoadjuvant Platform for Preoperative Immunotherapy

The persistent immunosuppression and spatial heterogeneity of advanced solid tumors necessitate next-generation neoadjuvant platforms capable of reprogramming tumor microenvironments while overcoming resistance to immune checkpoint blockade. Addressing this unmet clinical challenge, we report a {beta}-glucan-empowered nano-neoadjuvant agents (NNAs) engineered through topology-guided supramolecular assembly of pathogen-mimetic {beta}-glucan motifs onto photoresponsive single-wall carbon nanotubes. This biomimetic architecture capitalizes on three synergistic mechanisms: (1) Dectin-1-mediated pathogen-associated molecular pattern recognition to rewire myeloid cell functionality, (2) endogenous leukocyte-hitchhiking delivery paradigm, and (3) spatiotemporally controlled photothermal ablation via near-infrared transducing SWNT cores. NNAs also orchestrates a proinflammatory cascade involving IL-12-dependent Th1 polarization and activation, effectively converting "cold" tumors into immunogenic niches. This strategy redefines preoperative therapeutic paradigms, offering a multimodal platform to harness the proinflammatory adjuvant effect of SWNTs for preoperative immunomodulation in advanced-stage malignancies. By bridging innate immune recognition with nanotechnology-enabled precision, this paradigm establishes a new roadmap for preoperative conditioning of advanced malignancies, offering a theranostic framework to transform surgical outcomes through immunologically informed nanomedicine design.

immunology↗

Synaptic changes contribute to persistent extra-motor behaviour deficits in the rNLS8 TDP-43 mouse model of amyotrophic lateral sclerosis

Extra-motor symptoms are increasingly recognised in amyotrophic lateral sclerosis (ALS), encompassing cognitive, social, and behavioural deficits that can substantially impact quality of life. TAR DNA binding protein 43 (TDP-43) pathology is the central disease marker of almost all cases of ALS and approximately half of all frontotemporal dementia (FTD). However, the mechanisms linking TDP-43 pathology with extra-motor symptoms in TDP-43-associated neurodegenerative diseases remain unresolved. In this study, we used the rNLS8 mouse model, which expresses human TDP-43 with an ablated nuclear localisation sequence (hTDP-43∆NLS) in a doxycycline-regulatable manner causing progressive motor decline reminiscent of ALS, to delineate the molecular changes associated with disease-relevant phenotypes. We found that in addition to previously reported dramatic motor decline, rNLS8 mice also develop extra-motor phenotypes consistent with FTD, including disinhibition-like and anxiety-like behaviours, and social interaction impairments. These changes began in the earliest disease stages and remained readily detectable even when rNLS8 mice became severely motor impaired. Notably, extra-motor deficits persisted in rNLS8 mice that had recovered motor function upon hTDP-43∆NLS transgene suppression, regardless of whether recovery was initiated at timepoints prior to or after overt neurodegeneration begins. Transcriptomic analysis of rNLS8 mouse cortex tissues revealed early alterations in expression of 321 genes, most notably involving neuroinflammatory-related pathway activation, and all but 2 of these genes returned to control levels upon suppression of hTDP-43∆NLS expression. Further, 814 genes showed differential exon usage, indicating changes in alternative splicing, in rNLS8 mouse cortex. Of these, differential exon usage of 10 neuronal genes persisted after hTDP-43∆NLS transgene suppression, including synapse component genes Nrxn1, Unc13a, and Gls. Similarly, proteomics analysis of the cortex of rNLS8 mice revealed depletion of synaptic proteins, particularly those involved in glutamatergic signalling pathways, which also persisted following hTDP-43∆NLS transgene suppression. Similar glutamatergic pathway changes were detected in human ALS and FTD post-mortem cortex tissues. Our findings indicate that extra-motor phenotypes emerge early in disease in rNLS8 mice and remain evident despite progressive motor impairments. Further, extra-motor phenotypes persist even upon motor recovery, correlating with specific synaptic gene expression and splicing changes. Overall, this study suggests the potential utility of an expanded suite of behavioural paradigms in preclinical testing using rNLS8 mice, with enhanced relevance to the diversity of TDP-43 proteinopathies including FTD. Our findings further suggest that targeting glutamatergic synaptic components may be an avenue to correct extra-motor deficits associated with TDP-43 pathology.

neuroscience↗

Cryo-ET of IgG bivalent binding on SARS-CoV-2 provides structural basis for antibody avidity

The bivalent nature of IgG enhances its neutralization potency against enveloped viruses; however, on-virion structural details of IgG bivalent binding with antigens remain elusive. Here we used cryo-ET to investigate how two potent IgGs P17 and S309 interact with S-trimers on the SARS-CoV-2 surface. We found that these antibodies exploit the mobility of S-trimers to form diverse bivalent binding patterns. P17 stabilizes S-trimers in a one-RBD-up conformation and gathers S-trimer into linear multimers within minutes, whereas S309 primarily forms circular S-trimer assemblies that extend into lattice-like structures. Additionally, both IgGs can facilitate inter-virion coupling through bivalent binding of opposing S-trimers. These findings provide a structural basis for understanding IgG avidity and offer insights for antibody engineering and vaccine design.

biophysics↗

mTOR regulates Wnt signaling to promote tension-mediated lens vesicle closure

Lens vesicle closure is a pivotal event in ocular morphogenesis, and its disruption underlies Peters anomaly, a leading congenital cause of corneal opacity. Here, we elucidate a mechanistic hierarchy in which mTOR-Wnt signaling orchestrates cytoskeletal tension to drive this process. Conditional ablation of mTOR in the lens ectoderm induces aberrant corneal-lenticular stalk formation and transdifferentiation of the ciliary margin into neural retina. mTOR inhibition suppresses Wnt3 expression, and Wnt3 displayed a similar lens stalk phenotype, positioning mTOR as an upstream regulator of Wnt ligand production. Complete ablation of lens-derived Wnt ligands via deletion of the Wnt transporter Wls exacerbates developmental defects, triggering anterior lens herniation and ciliary margin development failure. Disruption of {beta}-catenin-mediated Wnt signaling or dual deletion of Wnt co-receptors Lrp5/6 in lens ectoderm similarly prevents vesicle closure, recapitulating lens herniation. Strikingly, Rac1 deletion rescues corneal-lenticular stalk phenotypes in mTOR, Wls, and {beta}-catenin mutants, directly linking Wnt effectors to cytoskeletal remodeling. Our findings establish an mTOR-Wnt-Rac1 signaling axis as the core regulator of cytoskeletal tension required for lens vesicle closure.

developmental biology↗

Unraveling the Neurocognitive Mechanisms of Delayed Punishment in Second- and Third-Party Contexts

Second-party punishment (SPP) and third-party punishment (TPP) are essential in regulating social behavior and maintaining social norms, yet the effectiveness may wane when punishment is delayed. Currently, the decision-making and neural mechanisms underlying SPP and TPP under temporal delays remain largely unexplored. This study investigated both SPP and TPP punishment decisions with time-delay (immediate vs. delayed) using a hypothetical criminal scenario assessment task with fMRI. Results showed increased activity in the bilateral precuneus and left temporoparietal junction (TPJ) and stronger left TPJ-dorsolateral prefrontal cortex (dlPFC) connectivity in SPP compared to TPP. Interestingly, third-parties imposed more severe punishment in delayed conditions than in immediate ones, accompanied by enhanced neural activity in dorsomedial prefrontal cortex (dmPFC), left TPJ, ventrolateral prefrontal cortex (vlPFC), ventromedial prefrontal cortex (vmPFC), and caudate nucleus. This delay effect was evident only in misdemeanor and felony cases, with no differences in capital offenses, suggesting a moderating effect of criminal severity. In contrast, SPP showed no significant changes in punishment or neural response across immediate and delayed conditions. Multivariate pattern analysis further indicated that dmPFC, TPJ, vlPFC, vmPFC and caudate function together to encode punishment severity in TPP contexts, a pattern not observed in SPP. These findings underscore distinct decision-making mechanisms between SPP and TPP under temporal delays, with implications for understanding justice-related processing in the human brain under time constraints. Significance statementWithin the justice system, punishing norm violators is often hindered when they flee, resulting in delayed punishments. However, little is known about how second-party (SPP) and third-party (TPP) implement punishment with time delays. The current study investigated this using real criminal scenarios with time delays under fMRI scanning. We found that third parties imposed more severe punishment on defendants in delayed conditions than in immediate ones, reflected by enhanced neural activity in the dorsomedial prefrontal cortex, left temporoparietal junction, ventrolateral prefrontal cortex, ventromedial prefrontal cortex, and caudate nucleus. In contrast, no significant differences were observed in second-party punishment. We also found a moderating effect of criminal severity: the difference between immediate and delayed sanctions by third-parties was present in misdemeanor and felony cases but not in capital offenses. These results shed light on the decision-making mechanisms of SPP and TPP in contexts involving temporal delay, which may have deep impact in different disciplines, e.g., social science, cognitive neuroscience and legal system.

neuroscience↗

Coro1a promotes the multivesicular body and plasma membrane fusion by facilitating PKM2-mediated SNAP-23 phosphorylation

During the formation of endosomal pathway-dependent extracellular vesicles (EVs), intraluminal vesicles in multivesicular bodies (MVBs) fuse with the plasma membrane (PM), releasing intraluminal vesicles to produce exosomes. Soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex, membrane fusion effector, is essential in this process. However, which SNARE complex is involved in MVB and PM fusion and how its assembly is regulated remain elusive. We have demonstrated that neddylation of Coro1a inhibits EV secretion by inducing Rab7-mediated degradation of MVBs. Here, we find that Coro1a increases EV biogenesis by promoting the assembly of SNARE complex STX-12-SNAP-23-VAMP-7 in a neddylation-independent manner. Coro1a activates PKM2 to enhance SNAP-23 phosphorylation in the presence of neddylation inhibitor MLN4924, which drives SNAP-23 to recruit more STX-12 and VAMP7, leading to increased formation of the STX-12-SNAP-23-VAMP-7 complex. Correspondingly, Coro1a-induced EV biogenesis is eliminated by PKM2 inhibitor or SNAP-23 silencing independent of neddylation. Reduced EVs from tumors due to Coro1a knockout cannot be observed in MLN4924-treated tumor mice with PKM2 inhibitor treatment either. Furthermore, Coro1a increases in tumor tissues from lung tumor patients with tumor progression, and high Coro1a indicates unfavorable survival of tumor patients, suggesting that increased Coro1a-mediated enhanced EV production from tumors accelerates tumor progression. Altogether, our data demonstrate that Coro1a facilitates EV biogenesis by promoting the assembly of STX-12-SNAP-23-VAMP-7 complex during MVB and PM fusion independent of neddylation, thereby being involved in the progression of EV-related diseases.

cell biology↗

Lysogen formation governs colonies while lytic infection is more prevalent in single cells of the bloom-forming cyanobacterium, Microcystis

While the bloom-forming cyanobacterium Microcystis can exist as free-living single cells or within dense mucilaginous colonies, the drivers and consequences of colony formation remain unclear. Here, we integrated metatranscriptomic datasets from two Microcystis bloom events in Lake Taihu, China, to analyze and validate the functional differences between colonial and single-cell Microcystis. Our results confirmed colony expression profiles were disproportionately enriched in Microcystis transcripts (and functions) compared to other prokaryotic taxa. Concomitantly, viral infection strategies diverged by Microcystis community morphology: colony-associated cells expressed lysogeny-associated genes, while single cells exhibited increased signatures of lytic infection. These data are consistent with the hypothesis that Microcystis colonies foster conditions favorable to lysogen formation--likely due to local high cell densities and the resulting advantage of superinfection immunity--whereas solitary cells experience stronger lytic pressure. On a broader scale, our findings refine the understanding of bloom dynamics by identifying how community morphological states coincide with distinct host-virus interactions. Cumulatively, this work underscores the importance of colony formation in shaping Microcystis ecology and highlights the need for mechanistic studies that disentangle the interplay between phage infection modes, colony formation, and microbial community structure.

microbiology↗

Perception and neural representation of intermittent odor stimuli in mice

Odor cues in nature are sparse and highly fluctuating due to turbulent transport. To investigate how animals perceive these intermittent cues, we developed a behavioral task in which head-restrained mice made binary decisions based on the total number of discrete odor pulses presented stochastically over several seconds. Mice readily learned this task, and their performance was well-described by widely used decision models. Logistic regression of binary choices against the timing of odor pulses within the respiratory cycle revealed that mice placed higher perceptual weight to stimuli arriving during inhalation than exhalation, a phase dependency that strongly correlated with the magnitude of responses in olfactory sensory neurons. The population response of anterior piriform cortex (APCx) neurons to odor pulses was also modulated by respiration phase, although individual neurons displayed varying levels of phase-dependence. Single APCx neurons responded stochastically and transiently to odor pulses, leading to a representation that carries signatures of sensory evidence, but not its accumulation. Our study reveals that mice can integrate intermittent odor signals across dozens of breaths, but respiratory modulation of sensory inputs imposes limits on information acquisition that cortical circuits cannot overcome to improve behavior.

neuroscience↗

Neoadjuvant anti-4-1BB confers protection against spontaneous metastasis through low-affinity intratumor CD8+ T cells in triple-negative breast cancer

Neoadjuvant immunotherapy seeks to harness the primary tumor as a source of relevant tumor antigens to enhance systemic anti-tumor immunity through improved immunological surveillance. Despite having revolutionized the treatment of patients with high-risk early-stage triple-negative breast cancer (TNBC), a significant portion of patients remain unresponsive and succumb to metastatic recurrence post-treatment. Here, we found that optimally scheduled neoadjuvant administration of anti-4-1BB monotherapy was able to counteract metastases and prolong survival following surgical resection. Phenotypic and transcriptional profiling revealed enhanced 4-1BB expression on tumor-infiltrating intermediate (Tint), relative to progenitor (Tprog) and terminally exhausted (Tterm) T cells. Furthermore, Tint was enriched in low-affinity T cells. Treatment with anti-4-1BB drove clonal expansion of Tint, with reduced expression of tissue-retention marker CD103 in Tprog. This was accompanied by increased TCR clonotype sharing between paired tumors and pre-metastatic lungs. Further interrogation of sorted intratumor T cells confirmed enhanced T cell egress into circulation following anti-4-1BB treatment. In addition, gene signature extracted from anti-4-1BB treated Tint was consistently associated with improved clinical outcomes in BRCA patients. Combinatorial neoadjuvant anti-4-1BB and ablation of tumor-derived CXCL16 resulted in enhanced therapeutic effect. These findings illustrate the intratumor changes underpinning the efficacy of neoadjuvant anti-4-1BB, highlighting the reciprocity between local tissue-retention and distant immunologic fortification, suggesting treatment can reverse the siphoning of intratumor T cells to primary tumor, enabling redistribution to distant tissues and subsequent protection against metastases.

immunology↗

Follicular mural granulosa cells stockpile glycogen to fuel corpus luteum pre-vascularization

The corpus luteum (CL) arises from the luteinization of follicular granulosa cells (GCs) and theca cells, marked by rapid progesterone elevation and angiogenesis. Intriguingly, angiogenesis lags behind progesterone elevation, creating an avascular phase during which luteal cells must fuel intensive steroidogenesis without perfusion. How the avascular CL meets this energetic demand remains a mystery. Here, we reveal a novel cellular adaptive mechanism-GC energy storage (GCES)-that resolves this enigma. We demonstrate that upon luteinization initiation, GCs enter a metabolically quiescent state yet enhance glucose uptake via SLC2A1, converting the glucose into glycogen through the hCG (LH)-MAPK-RUNX1-Insulin signaling axis. Catabolism of this glycogen reserve supplies the energy required for the avascular CL, ensuring normal luteogenesis. GCES is evolutionarily conserved across species. Genetic or pharmacological disruption of GCES or glycogenolysis induces luteal insufficiency, whereas timely glucose administration enhances GCES, improving luteal function and optimize reproductive outcome in both mouse and ovine models. In human study, orally intake of glucose post-hCG significantly augments GCES and enhances progesterone production in women. These results advance luteal physiology by uncovering a universal reproductive principle with direct clinical implications.

developmental biology↗

Cisternostomy facilitates clearance of metabolic waste from cerebrospinal fluid in patients with traumatic brain injury

Decompressive craniotomy, a common intervention for traumatic brain injury (TBI), can fail to effectively alleviate patient symptoms. Cisternostomy, reported for cistern drainage in TBI patients, has shown efficacy in reducing intracranial pressure and clearing detritus resulting from brain hemorrhage. However, the mechanisms underlying its effectiveness remain largely unknown. Here, we utilized non-targeted metabolomics to analyze cerebrospinal fluid from cisterns alongside peripheral blood samples from TBI patients undergoing cisternostomy. Through a systematic comparison of the cisternal cerebrospinal fluid and blood plasma metabolomes, we identified multiple blood-enriched metabolites, including betaine, triethanolamine, and proline, that were efficiently cleared during the acute stage of TBI. Notably, two metabolites linked to arginine metabolism and the urea cycle, N8-acetylspermidine and N-acetylputrescine, showed significant reductions that correlated with improvements in the Glasgow Coma Scale. Our findings indicate that cisternostomy effectively removes blood-derived substances and aids the recovery of patients with acute-stage TBI.

neuroscience↗

A Novel Optimized Silver Nitrate Staining Method for Visualizing the Osteocyte Lacuno-Canalicular System

A 50% silver nitrate solution is commonly used to stain and characterize the osteocyte lacuno-canalicular system (LCS) in bone biology research. However, variability in reagent concentrations and types, along with inconsistent staining procedures, have limited the broader application of this method in osteocyte research. In this study, we present a novel optimized silver nitrate staining technique aimed at addressing these limitations. This new method utilizes a 1 mol/L silver nitrate solution in combination with a type-B gelatin-formic acid solution at various concentrations (0.05%-0.5% gelatin and 0.05%-5% formic acid, or 1%-2% gelatin and 0.1%-2% formic acid) in volume ratios of 4:1, 2:1, or 1:1, or a 0.5 mol/L silver nitrate solution at a 4:1 ratio. The staining process is carried out for 1 hour under ultraviolet light or 90 minutes under regular room light (or dark), followed by washing with Milli-Q water to terminate the reaction. We applied this new method to stain the osteocyte LCS in bone samples from different species and pathological bone models. The technique consistently produced clear, distinct staining patterns across all samples. Moreover, our novel method revealed a greater number of LCS compared to the traditional 50% silver nitrate solution. This suggests that the commonly used 50% silver nitrate method may disrupt or inadequately reveal the LCS in certain species, potentially leading to an underestimation of LCS density and number. In conclusion, our novel silver nitrate staining method provides a simpler and more cost-effective alternative to the traditional technique. By offering a more accurate and comprehensive analysis of the LCS across species, this approach has the potential to advance research on osteocyte morphogenesis, as well as the functional and evolutionary adaptations of the osteocyte LCS across different taxa.

pathology↗

Cell Type-Specific and Diabetic Kidney Disease-Associated Expression of Long Non-Coding RNAs in Human Kidneys

BackgroundLong non-coding RNAs (lncRNAs) play essential roles in cellular processes, often exhibiting cell type-specific expression and influencing kidney function. While single-cell RNA sequencing (scRNA-seq) has advanced our understanding of cellular specificity, past studies focus solely on protein-coding genes. We hypothesize that lncRNAs, due to their cell-specific nature, have crucial functions within particular renal cells and thereby play essential roles in renal cell function and disease. MethodsUsing single-nucleus RNA sequencing (snRNA-seq) data from kidney samples of five healthy individuals and six DKD patients, we explored the non-coding transcriptome. Cell type-specific lncRNAs were identified, and their differential expression in DKD was assessed. Integrative analyses included expression quantitative trait loci (eQTL), genome-wide association studies (GWAS) for estimated glomerular filtration rate (eGFR), and gene regulatory networks. Functional studies focused on TARID, a lncRNA with podocyte-specific expression, to elucidate its role in podocyte health. Resultswe identified 349 lncRNAs with cell type-specific expression across kidney cell types. Of these, 104 lncRNAs were differentially expressed in DKD. Integrative analyses, including eQTL data, GWAS results for eGFR and gene regulatory networks, pinpointed TARID, a podocyte-specific lncRNA, as a key candidate upregulated in DKD. Functional studies confirmed TARIDs podocyte-specific expression and revealed its central role in actin cytoskeleton reorganization, a critical process in podocyte health. ConclusionsOur study provides a comprehensive resource of single-cell lncRNA expression in the human kidney and highlights the importance of cell type-specific lncRNAs in kidney function and disease. Specifically, we demonstrate the functional relevance of TARID in podocyte health. This work underscores the utility of integrating scRNA-seq with functional genomics to uncover novel regulatory mechanisms in kidney biology. Key pointsO_LIThis provides a resource for kidney (cell type-specific) lncRNA expression and demonstrates the importance of lncRNAs in renal health. C_LIO_LIWe identified 349 cell type-specific lncRNAs in the human kidney, with 104 showing altered expression in diabetic kidney disease (DKD). C_LIO_LITARID, a podocyte-specific lncRNA upregulated in DKD, is crucial for actin cytoskeleton reorganization in podocytes. C_LI

bioinformatics↗

Fusobacteria nucleatum determines the expression of amphetamine-induced behavioral responses through an epigenetic phenomenon.

Amphetamines (AMPHs) are psychostimulants commonly used for the treatment of neuropsychiatric disorders. They are also misused (AMPH use disorder; AUD), with devastating outcomes. Recent studies have implicated dysbiosis in the pathogenesis of AUD. However, the mechanistic roles of microbes in AUD are unknown. Fusobacterium nucleatum (Fn) is a bacterium that increases in abundance in both rats and humans upon AMPH exposure. Fn releases short-chain fatty acids (SCFAs), bacterial byproducts thought to play a fundamental role in the gut-brain axis as well as the pathogenesis of AUD. We demonstrate that in gnotobiotic Drosophila melanogaster, colonization with Fn or dietary supplementation of the SCFA butyrate, a potent inhibitor of histone deacetylases (HDACs), enhances the psychomotor and rewarding properties of AMPH as well as its ability to promote male sexual motivation. Furthermore, solely HDAC1 RNAi targeted inhibition recapitulates these enhancements, pointing to a specific process underlying this Fn phenomenon. Of note is that the expression of these AMPH behaviors is determined by the increase in extracellular dopamine (DA) levels that result from AMPH-induced reversal of DA transporter (DAT) function, termed non-vesicular DA release (NVDR). The magnitude of AMPH-induced NVDR is dictated, at least in part, by DAT expression levels. Consistent with our behavioral data, we show that Fn, butyrate, and HDAC1 inhibition enhance NVDR by elevating DAT expression. Thus, the participation of Fn in AUD stems from its ability to release butyrate and inhibit HDAC1. These data offer a microbial target and probiotic interventions for AUD treatment.

neuroscience↗

Gut meta-virome reveals potential zoonotic pathogens and environmental RNA viruses carried by non-human primates

The majority of human infectious diseases originate from mammals and are inherently zoonotic. Non-human primates (NHPs) are not only carriers of many zoonotic pathogens, but also the best intermediary for virus shift from harmless to harmful due to their similar phylogenetic relationship with humans. Knowledge of NHP viral composition and its underlying information can therefore provide an assessment of the risk of cross-species transmission and spillover of zoonotic diseases. However, studies that have successfully eliminated the effects of different natural habitat environments on viral carriage have been limited, making it difficult to identify which zoonotic viruses and potentially species-barrier-crossing viruses are carried by widely distributed NHP hosts. Here, we analyze viruses excreted in feces from NHP hosts and reveal the presence of possible zoonotic pathogens. Most of the viruses found come from plants that are eaten by them. Analysis of the evolutionary relationships of potential pathogens suggests that other clinical isolates are genetically correlated to HIV, PBV, and EV we identified. This study provides foundational data for surveillance of NHP enteroviruses that could help to be challenging to track potential human viruses carried by NHP in the absence of clinical surveillance. ImportanceAs a result of internationalization and other factors, many viruses have broken through the limits of geographical units and spread into human society, causing many emerging and re-emerging infectious disease hazards. However, the virus spreads and is by no means infectious to humans overnight. There is a phenomenon of host shift, in which the virus does not necessarily cause disease in an intermediate host, but causes significant damage when transmitted to humans. We focus on captive non-human primates, close relatives of humans in cities, because the phenomenon of host shifts is related to both biological similarity and geographical proximity of the host. Primates may carry zoonotic viruses and viruses that are currently incapable of infecting humans but have evolved with pathogenic potential. In summary, comprehensive viral surveillance and screening of captive nonhuman primates is necessary.

ecology↗

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↗