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Hussain, S.

Publications and source records attributed to Hussain, S..

At least 19 recordsLinked to original sources

Spatially-resolved multimodal profiling identifies functionally-heterogeneous cancer-associated fibroblasts associated with poor radiotherapy outcomes in muscle-invasive bladder cancer.

Background: Cancer-associated fibroblasts (CAFs) contribute to systemic therapy resistance in muscle-invasive bladder cancer (MIBC), but their functional heterogeneity and relevance to curative bladder-preserving radiotherapy, are poorly understood. Methods: Transcriptomic analysis was performed on 279 tumours from BC2001, a phase 3 radiotherapy clinical trial. To study CAF heterogeneity, we integrated bulk RNA-seq, single-cell spatial analysis of multiplex immunofluorescence images and quantification of extracellular matrix (ECM) features in 155 MIBC biopsies. The functional heterogeneity of distinct CAF populations was evaluated by single-nuclear RNA-seq. Spatial interactions between CAF populations and CD8+ T-cells was assessed and the relevance of lymphocytes to radiation responses was evaluated in a CAF-enriched murine bladder cancer model (BBN963). Results: BC2001 patients with CAF-enriched tumours had worse overall survival (HR=1.671, 95% CI 1.221-2.287, Log-rank p=0.0012). CAF abundance and antigen expression was highly heterogenous. Podoplanin (PDPN) was expressed on the majority of CAFs and was associated with inflammatory pathways. Enrichment of CAF gene signatures was associated with a significant increase in CAFs expressing fibroblast activation protein (FAP) (p=0.004) and dense ECM features (p=0.0004). Fifty-three percent of tumours exhibited stromal CD8+ T-cell exclusion with significant enrichment in FAP-dominant neighbourhoods (p<0.001). In vivo, lymphocytes were critical for radiation-induced tumour control, indicating that immune cold or excluded tumours may have limited radiotherapy responses. Conclusion: In MIBC, CAFs are associated with poor radiotherapy outcomes. Multiple mechanisms are deployed by functionally-heterogeneous CAFs, including promotion of chronic inflammation by PDPN+ CAFs and ECM remodelling by FAP+ CAFs which impact CD8+ T-cell distribution and radiation responses.

cancer biology↗

The Fontan EV Score: A Circulating Extracellular Vesicle-Based Risk Stratification Tool for Fontan-Associated Liver Disease

BackgroundFontan-associated liver disease (FALD) is a universal complication of the Fontan palliation characterized by chronic congestion and progressive hepatic fibrosis. Current diagnostics rely on invasive biopsies or non-specific biochemical and imaging biomarkers that fail to capture early fibrogenesis, creating a critical need for non-invasive biomarkers to stratify disease severity. MethodsWe utilized a translational ovine Fontan model (n = 19) to investigate circulating serum extracellular vesicles (sEVs) as reporters of hepatic pathology. Longitudinal serum samples paired with liver elastography were collected, and sEVs were subjected to multi-omic profiling including small RNA sequencing and proteomics. Regularized regression was used to identify transcriptomic predictors, which were integrated with time post-surgery into an ordinal logistic regression framework to construct the Fontan EV Score (FES). Model performance was evaluated on a held-out test cohort and benchmarked against established serological fibrosis indices. To validate the biological relevance of the FES panel, TGF-{beta}-treated human liver organoids were generated and scored miRNA expression was assessed. ResultsThe sEV proteome exhibited robust separation by surgical physiology, while the small RNA cargo was primarily stratified by fibrotic status. Bioinformatic analysis confirmed a high hepatic origin for these transcripts and identified enrichment of inflammatory pathways including Toll-like receptor and Interleukin-17 cascades in fibrotic subjects. The FES, incorporating time post-surgery and eleven small RNA biomarkers, demonstrated high predictive accuracy in the independent testing cohort with an AUC of 0.876 for moderate and 0.963 for severe fibrosis, substantially outperforming APRI (AUC = 0.618) and FIB-4 (AUC = 0.731). In TGF-{beta}-treated human liver organoids, several scoring miRNAs, including miR-125a-5p and miR-193b-5p, were directionally responsive to profibrotic stimulation. ConclusionsCirculating sEVs carry a liver-associated molecular cargo that can be leveraged for the non-invasive prediction of FALD severity. The FES provides a biologically validated scoring system that substantially outperforms existing serological indices and offers a new avenue for early detection and risk stratification of FALD Novelty and SignificanceO_ST_ABSWhat is Known?C_ST_ABSO_LIFontan-associated liver disease (FALD) is a nearly universal consequence of the Fontan circulation, driven by chronic venous hypertension and reduced cardiac output. C_LIO_LICurrent surveillance tools, including transaminases, composite serological indices (APRI, FIB-4), and elastography, have limited sensitivity and specificity for detecting and staging hepatic fibrosis in the Fontan population. C_LIO_LICirculating small extracellular vesicles (sEVs) carry tissue-derived molecular cargo and have shown diagnostic potential in other liver diseases, but their utility in FALD has not been explored. C_LI What New Information Does This Article Contribute?O_LIMulti-omic profiling of circulating sEVs in a translational ovine Fontan model reveals that the small RNA cargo is stratified by fibrotic status and enriched for inflammatory pathways associated with hepatic stellate cell activation. C_LIO_LIThe Fontan EV Score (FES), integrating time post-surgery with eleven circulating small RNA biomarkers, predicts FALD severity with substantially greater accuracy than APRI and FIB-4. C_LIO_LITGF-{beta}-treated human liver organoids confirm that several FES-associated miRNAs are directly responsive to profibrotic stimulation, providing biological validation independent of Fontan hemodynamics. C_LI This study demonstrates that circulating sEVs function as non-invasive reporters of hepatic fibrogenesis in the Fontan circulation and introduces the first EV-based scoring system for FALD risk stratification. The FES achieved an AUC of 0.876 for moderate and 0.963 for severe fibrosis in an independent test cohort, outperforming established serological indices that were originally developed for viral hepatitis but which perform poorly in congestive hepatopathy. By combining molecular biomarker discovery with in vitro functional validation, this work establishes a foundation for developing targeted, non-invasive diagnostics to guide surveillance and clinical decision-making in the growing Fontan patient population.

bioinformatics↗

First Genome-Scale Metabolic Model for Understanding HMPV-Host Interaction

BackgroundHuman Metapneumovirus (HMPV) is a major contributor to acute respiratory tract infections. Currently, no approved vaccines or specific antiviral therapies are available worldwide. Genome-scale metabolic models (GEMs), when integrated with Viral Biomass Objective Functions (VBOFs), provide a robust computational framework for identifying host metabolic dependencies essential for viral replication. This approach enables systematic prioritization of potential antiviral drug targets. ResultsThe first comprehensive VBOF for HMPV was constructed by integrating stoichiometric data from the viral genome, including structural proteins with defined copy numbers, amino acid residues per virion, envelope lipids, and glycan modifications. The reconstructed VBOF was incorporated into the human bronchial epithelial cell model, iHBEC1, to analyze metabolic changes between uninfected and infected host cells. Knockout analysis identified two selective antiviral gene targets: PGM3 (phosphoacetylglucosamine mutase) and GNPNAT1 (N-acetylglucosamine-6-phosphate acetyltransferase), as well as seven selective reaction targets primarily within the hexosamine biosynthesis and nucleotide sugar pathways. Knockout of PGM3 or GNPNAT1 completely abolished viral production while preserving complete host cell viability. Additionally, guanylate kinase (GUK1/GK1) emerged as a highly selective target for HMPV, confirming findings from Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) studies and suggesting a conserved vulnerability across respiratory viruses. ConclusionsUDP-GlcNAc, the vital end-product of the hexosamine biosynthesis pathway (HBP), is computationally predicted as a critical metabolic hub. This pathway represents the primary metabolic vulnerability of HMPV, due to the extensive glycosylation requirements of the HMPV attachment protein. The host-directed antiviral targets PGM3 and GNPNAT1 are high-priority candidates for experimental validation and may provide novel strategies to combat this respiratory infection.

Systems Biology↗

CD163 protects against pulmonary injury and inflammation induced by acute O3 exposure

Ozone (O3)-driven pulmonary inflammation is partly regulated by damage associated molecular patterns (DAMPs) binding to scavenging receptors (SRs). However, how SRs and DAMPs regulate O3-induced pulmonary inflammation remains incompletely understood. CD163 is a SR responsible for clearing cell free hemoglobin (CFH), a DAMP which accumulates during acute pulmonary injury and is associated with worsening respiratory outcomes. We hypothesized that increased CD163 is necessary for reducing CFH levels and resolving O3-induced pulmonary injury. To test this hypothesis, we defined CD163 and CFH responses to O3 exposure in C57BL/6N (WT) and CD163 deficient (Cd163-/-) mice, as well as in human bronchoalveolar lavage fluid (BALF). In WT mice, lung Cd163 expression was significantly increased by O3 during peak inflammation and declined 24 hours post exposure. Human exposure studies revealed a diversity of Cd163 expression and a reduction of CFH following O3 exposure, suggesting regulation of this pathway in humans. When compared to WT mice, Cd163-/- mice had augmented O3-induced pulmonary injury, inflammation, and oxidative stress. Further, the antioxidant EUK-134 did not reduce O3-induced pulmonary oxidative stress in Cd163-/- mice, suggesting a role for CD163 in the pulmonary response to oxidative insults. Furthermore, compared to WT controls, Cd163-/- mice receiving an oropharyngeal aspiration of CFH had a significant increase in airspace inflammation. Combined, these findings suggest that CD163 mediated clearance of CFH is involved in resolving O3-induced pulmonary injury, inflammation, and oxidative stress. New & NoteworthyOzone (O3) is known to induce damage associated molecular patterns (DAMPs) which drive lung inflammation. The scavenging receptor, CD163, binds and clears the DAMP cell free hemoglobin (CFH), which accumulates during sterile lung injury. Our findings indicate that O3 exposure alters CD163 expression in the lung and that mice lacking Cd163 expression have more lung inflammation. Our data indicate that CD163 serves a protective role in response to acute O3 exposure perhaps through CFH clearance.

pharmacology and toxicology↗

Filling surveillance gaps: Bayesian INLA models for predicting tick distributions in data-sparse regions

Fragmented and geographically uneven surveillance limits the ability to target tick monitoring and control in many livestock systems. We evaluated whether heterogeneous published surveillance could be converted into district-level, uncertainty-aware abundance predictions for Rhipicephalus microplus and Hyalomma anatolicum across Punjab and Khyber Pakhtunkhwa, Pakistan. Species-specific tick counts were standardized by the number of animals examined and sampling duration and expressed as ticks per 100,000 animal-months. Environmental covariates were summarized using principal component analysis, with livestock density included separately. Bayesian Gaussian models, with and without a district-level Besag-York-Mollie 2 spatial effect, were fitted in R using Integrated Nested Laplace Approximation (INLA) and compared. Leave-one-district-out validation was performed to assess out-of-sample predictive performance. Spatial models improved model fit for both species. For R. microplus, PC1 and PC4 showed credible negative associations with abundance, whereas no fixed-effect 95% credible interval excluded zero for H. anatolicum. Predicted R. microplus abundance was more spatially heterogeneous, with high but uncertain estimates in several northern districts, whereas H. anatolicum predictions were more homogeneous and relatively higher toward southern Punjab. Mapping posterior uncertainty identified districts where additional standardized surveillance would be most informative. This approach provides a transferable framework for extracting spatial surveillance information from heterogeneous veterinary data while explicitly representing uncertainty.

ecology↗

Gut microbiota within-host evolution enforces colonization resistance against enteric infection

Limited resource availability in the gut promotes competitive interactions between bacteria, which drive adaptive within-host evolution (1-3). While adaptive evolution of bacterial communities has been increasingly studied in the recent years (4-7), its functional implications for host physiology remain unknown. Here, we show that within-host evolution of the human commensal Enterococcus faecalis boosts colonization resistance to enteric Salmonella enterica serovar Typhimurium (S. Typhimurium) infection. During gut colonization, E. faecalis evolves the ability to metabolize fructoselysine, an abundant Amadori rearrangement product generated by thermal food processing. The depletion of this diet-derived nutrient prevents S. Typhimurium colonization by restricting an essential resource. This protective mechanism was conserved across independent mouse colonies and arises via diverse evolutionary trajectories, including nucleotide polymorphisms, gene amplifications, and a horizontal gene transfer event. Additionally, analysis of E. faecalis isolates from human infants revealed that adaptation to fructoselysine availability occurs in a diet-dependent manner. Isolates from infants fed with fructoselysine-rich formula were able to utilize fructoselysine, whereas those from infants fed with fructoselysine-poor breast milk were not. Conclusively, our results identify an inherent microbiome-driven self-healing mechanism, wherein bacterial evolution restores colonization resistance against enteric pathogens through evolved nutrient depletion. Understanding these evolutionary dynamics will inform microbiome-targeted approaches to prevent and treat infectious diseases by harnessing adaptive bacterial metabolism.

microbiology↗

Programmed strain tagging and gene disruption throughout a diverse bacterial genus

Transposons are a convenient vehicle for inserting DNA into a bacterial genome, but widely-used transposons such as Tn7, Tn5, and Mariner do not hit custom targets. Recently, CRISPR-associated transposons (CASTs) have been developed as tools to direct the insertion of a transposon to a chosen site with a short guide sequence. We adapted this system for use in the widespread plant-associated genus Sphingomonas, uniquely tagging genetically diverse strains in several different sites, and we demonstrate the utility of the tags for quantitative strain tracking in complex bacterial populations. Although we initially targeted the conserved site into which Tn7 integrates as a benign transposition location, a genomics search revealed insertions at this site would frequently disrupt genes not only in Sphingomonas but also in widely studied Pseudomonas. Therefore we identified improved genus-wide conserved sites between convergently terminating genes as alternatives. We experimentally validated an improved neutral site in Sphingomonas, and then targeted this site in a heterogeneous uncharacterized Sphingomonas population. Using a tagIM seq, a novel rapid transposon mapping method introduced here, we screened resulting transformant colonies for off-target transposon insertions. This enabled prioritization of correctly tagged novel strains, accelerating the creation of fully tagged synthetic communities for the high-throughput study of fine-scale bacterial natural variation.

microbiology↗

BRG1 cooperates with PLK1 to regulate dormant origin activation during S phase.

The ATP-dependent chromatin remodeler BRG1 is well-established in the regulation of gene expression, DNA replication, homologous recombination, DNA damage repair, and apoptosis. While its genome-wide occupancy has primarily been linked to transcriptional regulation, its potential role in DNA replication control remains less well defined. In this study, we investigated BRG1s involvement in replication origin regulation by integrating BRG1 ChIP-seq data with replication origin mapping and chromatin state analyses. Our results revealed that BRG1 is preferentially enriched at genomic regions characterized by DNase I hypersensitivity, low GC content, and a capacity to form G-quadruplex structures hallmarks of dormant replication origins. Notably, BRG1-bound sites were also enriched in late-replicating, heterochromatic regions. These findings suggest a specific association of BRG1 with dormant replication origins. To validate this association, we performed functional assays in HeLa cells. BRG1 depletion via siRNA led to reduced replication fork progression and increased activation of dormant origins, consistent with replication stress. Mechanistically, we found that BRG1 physically interacts with the mitotic kinase PLK1. Loss of BRG1 reduced chromatin-bound levels of both BRG1 and PLK1, implicating BRG1 in PLK1 recruitment or stability. Importantly, overexpression of PLK1 in BRG1-depleted cells rescued replication fork progression, supporting a cooperative role for BRG1 and PLK1 in regulating replication through dormant origins. Together, these data uncover a previously unrecognized function for BRG1 in the selective regulation of dormant replication origin firing, acting in concert with PLK1.

molecular biology↗

Knowledge, attitudes, and practices of para-veterinary workers about ticks and tick-borne diseases in three provinces of Pakistan

There is a high prevalence of tick infestation in Pakistani livestock, affecting more than 45% of the population of more than 200 million small and large ruminants. Most livestock farmers seek assistance from para-veterinary workers, who fall under the definition of Veterinary Paraprofessionals (VPPs), according to the World Organization for Animal Health (WOAH). There is a shortage of information concerning the awareness of these para-veterinary workers regarding tick control and management. This study aims to bridge this critical knowledge gap by conducting a cross-sectional survey that evaluates the knowledge, attitudes, and practices of para-veterinary workers about tick-borne diseases (TBDs) in Pakistan. Between March and August 2023, we conducted a web-based survey among para-veterinary workers recruited via email, text message, and face-to-face conversations. Poisson regression was used to identify factors associated with knowledge, attitude, and practice (KAP) scores related to TBDs. We received 118 responses from three provinces; only 27.9% (n = 33) responded that they had attended workshops related to ticks and TBDs. Attending workshops was associated with higher KAP scores. All section scores were correlated, and higher knowledge scores were significantly associated with lower odds of tick exposure. Our findings suggest that workshop attendance is important in increasing overall awareness and promoting better practices regarding TBDs.

scientific communication and education↗

Endogenous glucocorticoids moderate the gastric inflammatory response to Helicobacter infection and protect from autoimmunity.

Background and AimsImmune responses to infection must balance pathogen clearance with minimizing tissue damage and autoimmunity. Chronic gastric inflammation caused by H. pylori damages the gastric mucosa and promotes carcinogenesis. Glucocorticoids are immunoregulatory hormones that limit immune activation in the stomach. This study aimed to determine how endogenous glucocorticoids regulate the gastric immune response to Helicobacter infection and their impact on preneoplastic lesion development. MethodsWe examined the role of endogenous glucocorticoids in shaping the gastric immune response to Helicobacter felis colonization. Gastric immune cell infiltration, atrophy, metaplasia, and preneoplastic lesion development were evaluated in adrenal-intact control mice and adrenalectomized (ADX) mice. Auto-reactive IgG antibodies were assessed using a mouse self-antigen array and by measuring their binding to healthy gastric tissue. ResultsLoss of endogenous glucocorticoids led to significantly increased H. felis-induced gastric T cell infiltration and proinflammatory cytokine expression compared to intact-infected controls. While all intact mice maintained chronic infection for up to 12 months, nearly all ADX mice eradicated H. felis within 2-3 weeks. Despite bacterial clearance, ADX mice continued to exhibit chronic gastric inflammation and developed dysplasia. Autoantibody profiling showed that both intact and ADX groups generated self-reactive IgG during active infection. However, only ADX mice sustained autoantibody production following bacterial eradication. ConclusionsEndogenous glucocorticoids attenuate gastric inflammation during Helicobacter infection, supporting bacterial persistence while maintaining immune tolerance. These findings suggest that heightened immune responses to H. pylori may trigger autoimmune gastritis (AIG) development, which can persist after H. pylori clearance and continue to drive gastric cancer risk.

immunology↗

Antimicrobial Loaded Graft-Copolymer Nanoparticles for Treatment of Pseudomonas aeruginosa Infections

Nearly 80% of cystic fibrosis patients are affected by persistent lung infections, with Pseudomonas aeruginosa being one of the major culprits. Treatment of P. aeruginosa is further complicated by its ability to form biofilms. Anionic compounds within the biofilm and thick cystic fibrosis mucus interact with cationic antimicrobials, hindering treatment efficacy. In this study, we investigated the treatment of lung infections by delivering antimicrobials via polyelectrolyte surfactants that are composed of an anionic poly(alkylacrylic acid) backbone with grafted polyetheramine pendent chains. When combined with cationic antimicrobials, they self-assemble into nanoparticles via electrostatic interactions. We assessed the role of backbone chemistry and graft density on nanoparticle physical properties and evaluated the antimicrobial activity of these formulations against planktonic and biofilm cultures of P. aeruginosa strains derived from clinical isolates. All synthesized polyelectrolyte surfactants demonstrated high levels of antimicrobial encapsulation, with the extent of drug bound corresponding to the calculated hydrophilic-lipophilic balance values. We observed significantly increased antimicrobial activity against planktonic cultures using nanoformulations containing one of the polyelectrolyte surfactants, PMAA-g-10%J. In contrast, all tested nanoformulations retained, but did not increase, activity against biofilms. By monitoring membrane potentials and nanoparticle uptake, it was found that the nanoparticles directly associate with the bacterial cell membranes, which may enhance drug delivery and underlie the improved activity against the planktonic bacteria. In conclusion, we provide a proof of concept for the design of polyelectrolyte surfactants for the nanoencapsulation and delivery of cationic drug cargoes against P. aeruginosa infections.

bioengineering↗

Liver-Derived, Circulating Xanthine Oxidoreductase Drives Vascular Impairment Associated with Inhalation of Ultrafine Particulates.

Inhalation of ultrafine particles (UFP) mediates systemic vascular impairment which is, in part, driven by elevated rates of oxidant generation. One significant source of oxidant production in the vascular compartment is the purine catabolizing enzyme, xanthine oxidoreductase (XOR). However, mechanisms linking XOR and/or endothelial glycosaminoglycan (GAG)-sequestered XOR to vessel dysfunction allied to UFP inhalation remain underexplored. Based on known interactions between UFP and the liver, we hypothesized that exposure could lead to hepatic release of XOR to the circulation which subsequently contributes to vascular impairment. Utilizing our murine hepatocyte-specific XOR knockout (XORHep-/-) model (loss of function) in conjunction with reintroducing exogenous XOR (restoration of function) we demonstrate a specific role for liver-derived XOR in the pathogenesis of UFP-induced vascular impairment. Exposure of mice as well as in vitro exposure of hepatocytes to our model UFP, nano titanium dioxide (nTiO2) results in the upregulation and active release of XOR. Drinking water supplemented with the XOR inhibitor febuxostat or nitrite (NaNO2-) partially prevented nTiO2-induced impairment of vascular reactivity. Interestingly, nitrite appears to cause a down-regulation of hepatic XOR. XORHep-/- mice were partially protected against both impairment of endothelial dependent dilation and augmented angiotensin II constriction. To further demonstrate the role of circulating XOR in nTiO2-induced impairment of vessel reactivity, XORHep-/- mice had circulating XOR restored by i.v. injection prior to exposure, which eliminated the protection of the hepatic knockout. It is important to note that acute restoration of intraluminal XOR in isolated vessels did not alter endothelial-dependent dilation or angiotensin II constriction. As such, we interrogated potential downstream mediators of XOR effects on endothelial function and found a decrease in the repressive trimethylation of lysine 9 on histone 3. Together these findings demonstrate that circulating XOR is a key contributor to endothelial dysfunction caused by UFP exposure. However, the impairment is not acute in nature and might involve epigenetic-mediated alterations in gene expression.

physiology↗

A neuroprotective tetrapeptide for treatment of acute traumatic brain injury

Traumatic brain injury (TBI) is a major clinical problem because of the high incidence and the severity of the subsequent sequelae. Despite extensive efforts, there are no therapeutic drugs clinically approved for treating acute TBI patients. To address this unmet need, we assessed the activity of the tetrapeptide, CAQK, in mice. When administered intravenously shortly after moderate or severe TBI, CAQK accumulates in the injured brain in mice and pigs. CAQK binds to an extracellular matrix glycoprotein complex that is upregulated in injured brain. Treatment of TBI mice with CAQK resulted in reduction in the size of the injury compared to control mice. There was reduced upregulation of the glycoprotein complex, less apoptosis, and lower expression of inflammatory markers in the injured area, indicating that CAQK alleviates neuroinflammation and the ensuing secondary injury. CAQK treatment also improved functional deficit in TBI mice, with no overt toxicity. Our findings suggest that CAQK may have therapeutic applications in TBI.

neuroscience↗

RNA Transcripts Serve as a Template for Double-Strand Break Repair in Human Cells

Double-strand breaks (DSBs) are toxic lesions that lead to genome instability. While canonical DSB repair pathways typically operate independently of RNA, emerging evidence suggests that RNA:DNA hybrids and transcripts near damaged sites can influence repair outcomes. However, a direct role for transcript RNA as a template during DSB repair in human cells is yet to be established. In this study, we designed fluorescent- and sequencing-based assays, which demonstrated that RNA-containing oligonucleotides and messenger RNA serve as templates to promote DSB repair. We conducted a CRISPR/Cas9-based genetic screen to identify factors that promote RNA-templated DSB repair (RT-DSBR), and of the candidate polymerases, we identified DNA polymerase-zeta (Pol{zeta}) as the potential reverse transcriptase that facilitates RT-DSBR. Furthermore, by analyzing sequencing data from cancer genomes, we identified the presence of whole intron deletions, a unique genomic scar reflective of RT-DSBR activity generated when spliced mRNA serves as the repair template. These findings highlight RT-DSBR as an alternative pathway for repairing DSBs in transcribed genes, with potential mutagenic consequences.

molecular biology↗

Interactive effect of Moringa oleifera mediated green nanoparticles and arbuscular mycorrhizal fungi on growth, root system architecture, and nutrient uptake in maize (Zea mays L.)

The synergistic interaction between green nanoparticles (NPs) and mycorrhizal fungi promotes plant growth by improving nutrient absorption, optimizing root function, and stress resistance. In this study, we explored the impact of arbuscular mycorrhizal fungus (AMF) Funnaliformis mosseae and Moringa oleifera mediated green NPs viz; iron oxide (FeO), zinc oxide (ZnO), and Zn doped FeO (Zn/Fe) NPs, both individually and in combination, on maize growth, root system architecture, organic acids production, mycorrhizal colonization, and nutrients uptake. Prior to NP synthesis, metabolomic analysis of Moringa oleifera leaves was conducted to characterize its bioactive compounds. The structural properties of green synthesized NPs confirmed by characterization using scanning electron microscopy (SEM), Fourier transform infrared (FTIR) spectroscopy, UV-Vis spectrophotometry, and X-ray diffraction (XRD). The results showed that all individual and combined treatments of AMF and green NPs significantly enhanced maize growth compared to the control. Among the single NP treatments, Zn/Fe NPs exhibited superior performance over FeO and ZnO. However, when combined with AMF, ZnO and Zn/Fe NPs induced the highest growth responses than FeO NPs. The ZnO NPs proved most compatibility with AMF for improving colonization in maize roots, whereas FeO and Zn/Fe NPs reduced colonization efficiency. Furthermore, combination of AMF and ZnO NPs (AMF+ ZnO) noted as most prominent treatment for improvement of maize growth compared to other all treatments, highlighting the potential of AMF+ ZnO NPs for sustainable agricultural applications.

plant biology↗

Personalized whole-brain activity patterns predict human corticospinal tract activation in real-time

BACKGROUNDTranscranial magnetic stimulation (TMS) interventions could feasibly treat stroke-related motor impairments, but their effects are highly variable. Brain state-dependent TMS approaches are a promising solution to this problem, but inter-individual variation in lesion location and oscillatory dynamics can make translating them to the poststroke brain challenging. Personalized brain state-dependent approaches specifically designed to address these challenges are therefore needed. METHODSAs a first step towards this goal, we tested a novel machine learning-based EEG-TMS system that identifies personalized brain activity patterns reflecting strong and weak corticospinal tract (CST) output (strong and weak CST states) in healthy adults in real-time. Participants completed a single-session study that included the acquisition of a TMS-EEG-EMG training dataset, personalized classifier training, and real-time EEG-informed single pulse TMS during classifier-predicted personalized CST states. RESULTSMEP amplitudes elicited in real-time during personalized strong CST states were significantly larger than those elicited during personalized weak and random CST states. MEP amplitudes elicited in real-time during personalized strong CST states were also significantly less variable than those elicited during personalized weak CST states. Personalized CST states lasted for [~]1-2 seconds at a time and [~]1 second elapsed between consecutive similar states. Individual participants exhibited unique differences in spectro-spatial EEG patterns between personalized strong and weak CST states. CONCLUSIONOur results show for the first time that personalized whole-brain EEG activity patterns predict CST activation in real-time in healthy humans. These findings represent a pivotal step towards using personalized brain state-dependent TMS interventions to promote poststroke CST function.

neuroscience↗

Spontaneous calcium transients in hair cell stereocilia

The hair bundle of auditory and vestibular hair cells converts mechanical stimuli into electrical signals through mechanoelectrical transduction (MET). The MET apparatus is built around a tip link that connects neighboring stereocilia that are aligned in the direction of mechanosensitivity of the hair bundle. Upon stimulation, the MET channel complex responds to changes in tip-link tension and allows a cation influx into the cell. Ca2+ influx in stereocilia has been used as a signature of MET activity. Using genetically encoded Ca2+ sensors (GCaMP3, GCaMP6s) and high-performance fluorescence confocal microscopy, we detect spontaneous Ca2+ transients in individual stereocilia in developing and fully formed hair bundles. We demonstrate that this activity is abolished by MET channel blockers and thus likely originates from putative MET channels. We observe Ca2+ transients in the stereocilia of mice in tissue explants as well as in vivo in zebrafish hair cells, indicating this activity is functionally conserved. Within stereocilia, the origin of Ca2+ transients is not limited to the canonical MET site at the stereocilia tip but is also present along the stereocilia length. Remarkably, we also observe these Ca2+ transients in the microvilli-like structures on the hair cell surface in the early stages of bundle development, prior to the onset of MET. Ca2+ transients are also present in the tallest rows of stereocilia in auditory hair cells, structures not traditionally thought to contain MET channels. We hypothesize that this newly described activity may reflect stochastic and spontaneous MET channel opening. Localization of these transients to other regions of the stereocilia indicates the presence of a pool of channels or channel precursors. Our work provides insights into MET channel assembly, maturation, function, and turnover.

cell biology↗

Chronic cigarette smoke exposure masks pathological features of Helicobacter pylori infection while promoting tumor initiation

Gastric cancer is the fifth most common cancer and the fifth leading cause of cancer deaths worldwide. Chronic infection by the bacterium Helicobacter pylori is the most prominent gastric cancer risk factor, but only 1-3% of infected individuals will develop gastric cancer. Cigarette smoking is another independent gastric cancer risk factor, and H. pylori-infected smokers are at a 2-11-fold increased risk of gastric cancer development, but the direct impacts of cigarette smoke on H. pylori pathogenesis remain unknown. In this study, male C57BL/6 mice were infected with H. pylori and began smoking within one week of infection. The mice were exposed to cigarette smoke (CS) five days/week for 8 weeks. CS exposure had no notable impact on gross gastric morphology or inflammatory status compared to filtered-air (FA) exposed controls in mock-infected mice. However, CS exposure significantly blunted H. pylori-induced gastric inflammatory responses, reducing gastric atrophy and pyloric metaplasia development. Despite blunting these classic pathological features of H. pylori infection, CS exposures increased DNA damage within the gastric epithelial cells and accelerated H. pylori-induced dysplasia onset in the INS-GAS gastric cancer model. These data suggest that cigarette smoking may clinically silence classic clinical symptoms of H. pylori infection but enhance the accumulation of mutations and accelerate gastric cancer initiation.

cancer biology↗