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Garg, S.

Publications and source records attributed to Garg, S..

At least 19 recordsLinked to original sources

Predicting alcohol consumption from resting-state functional connectivity: Feature relevance and the potential of meta-matching.

Alcohol use disorder (AUD) is among the most prevalent mental disorders. Associations between resting-state fMRI functional connectivity (FC) and AUD have been reported but rarely replicated. In this preregistered study, we investigated the extent to which FC predicts alcohol consumption, as measured by the AUDIT-C score, in a large sample of non-treatment-seeking alcohol consumers (N = 739), including 528 participants with varying degrees of AUD severity. To optimize performance, we compared kernel ridge regression (KRR) trained directly on this sample with transfer-learning models based on multilayer meta-matching embeddings, from which we derived data-driven relevance maps at the connection, region, and network levels. We tested split-half reliability, reproducibility across cohorts, and outcome specificity of the relevance maps. Both models predicted AUDIT-C scores moderately but significantly (r {approx} 0.15). Meta-matching did not outperform KRR in prediction. Relevance maps showed limited split-half reliability, consistent with the modest predictive performance, but reproduced moderately well across two independent cohorts. These maps indicate reduced connectivity among limbic regions, the anterior middle temporal gyrus, the dorsomedial prefrontal cortex, and dorsal attention network regions. In contrast, hypothesized hyperconnectivity patterns involving the striatum, anterior cingulate cortex, and precuneus were less reliable and mostly non-significant. Overall, our findings suggest that resting-state FC contains reproducible but weak signals related to alcohol consumption. Transfer learning improved relevance-map reliability but not prediction performance and reduced outcome specificity. These results support the utility of interpretable machine learning for identifying connectivity patterns related to drinking behavior, while also highlighting current limitations in its predictive power.

neuroscience↗

Altered Aperiodic EEG Activity in Adolescents with Neurofibromatosis Type 1

BackgroundThe balance between excitatory and inhibitory neuronal signalling (E/I balance), proposed as a key mechanism controlling neuronal activity, is disrupted in many neurodevelopmental conditions. One such condition is Neurofibromatosis Type 1, a monogenic neurodevelopmental disorder characterised by increased inhibitory tone. While previous research suggests that E/I balance may be altered in infancy, it is unknown whether E/I balance remains altered during adolescence in NF1. Here we investigated this question using the aperiodic exponent of the resting electroencephalogram (EEG) power spectrum, a proposed electrophysiological index of E/I balance. MethodThe aperiodic exponent of the EEG power spectrum ( 1/f) was estimated for 16 adolescents with NF1 diagnosis aged 11-16, and 16 age- and sex-matched neurotypical controls. General linear models (GLM) were fit to estimate effects of NF1 diagnosis, age and their interaction on aperiodic exponent. We also estimated the peak dominant frequency and power in oscillatory activity of the EEG signal and fitted the same structure of GLM models. Cognitive assessments across domains of memory, executive function and attention were also analysed with GLM to examine brain-cognition associations. ResultsThe NF1 group had higher aperiodic exponent compared to neurotypical controls, but the aperiodic exponent was not associated with cognitive performance. After accounting for aperiodic activity, the NF1 group also had lower dominant oscillatory frequency than the control group. There was no significant interaction between NF1 diagnosis and age on PAF. There were no group differences in peak alpha power. ConclusionsWe demonstrate for the first time that the alterations to aperiodic activity in NF1 are consistent with the proposed mechanism of increased inhibitory tone. These findings show the potential of this paradigm for future pharmacological and brain stimulation trials investigating treatment-related changes in cortical function.

neuroscience↗

Leukemic Stem Cell Subtypes Drive Distinct Niche Remodeling in Acute Myeloid Leukemia

Leukemic stem cells (LSCs) sustain acute myeloid leukemia (AML) and are implicated in therapy resistance and relapse. Yet, it remains unknown how LSCs remodel the bone marrow niche. AML is known to alter stromal and vascular microenvironments, but these effects are difficult to separate from bulk leukemic burden and immune inflammation. Here, we use isogenic human AML xenografts with distinct LSC characteristics but comparable engraftment to define LSC-associated niche remodeling in vivo. Single-cell profiling revealed that LSC-high AML shifts the mesenchymal niche toward fibro-inflammatory states, expanding Fmod+ fibroblasts and Cd34+ perivascular fibroblast-like cells while suppressing osteolineage differentiation. The leukemic compartment remained heterogeneous, with a specific MEP-like LSC population expressing niche-remodeling ligands including TGFB1, IL1B, and ANGPT1. LSC-high AML activated a TGF{beta}-responsive, CREB3L1-controlled fibroblast trajectory, and perturbing TGF{beta} signaling or CREB3L1 activation reduced stromal support for AML cells. These findings identify a specific LSC subtype as a source of niche-remodeling cues that shape specialized leukemia-supportive niches.

molecular biology↗

The Impact of Smoking Status on the Genomic Landscape of Lung Squamous Cell Carcinoma

PurposeComprehensive genomic profiling (CGP) has changed the treatment paradigm for non-small cell lung cancer (NSCLC) with the advent of molecularly targeted therapies for actionable genomic alterations (AGA). Despite this, the use of CGP is suboptimal, particularly in squamous cell lung cancer (sqNSCLC), which is more closely associated with smoking exposure and a lack of AGAs. We hypothesized that the prevalence of AGAs is inversely correlated with the chronicity and extent of smoking exposure in patients with sqNSCLC. Experimental DesignWe retrospectively evaluated all patients with liquid biopsy testing via Guardant 360CDX or Guardant360 in the context of any sqNSCLC diagnosis at the City of Hope Comprehensive Cancer Center between 10/2020 and 7/2023. The data was obtained on 2/23/24. Social and clinical histories were evaluated to assess the frequency of AGAs in patients with no or remote smoking history. ResultsOf the 56 patients in the initial evaluation, 24% (n=13) were non-smokers or remote smokers (greater than 20 years from cessation). Of these 13 patients, eight (61.5%) harbored AGA. Of these 8 patients, alterations observed included EGFR exon 19 deletion (50%, n=4), MET exon 14 skipping mutation (25%, n=2), EGFR G719S (13%, n=1), EGFR E114K (13%, n=1). Of those patients harboring AGAs that received NCCN-concordant matched targeted therapy, the objective response rate (ORR) with targeted agents was 50% and the clinical benefit rate (CBR) was 83.3%. ConclusionsThese data support the use of CGP in sqNSCLC particularly in patients with remote or no smoking exposure. Statement of translational relevanceThese data demonstrate high frequency of actionable genomic alterations (AGAs) in patients diagnosed with squamous cell lung cancer (sqNSCLC) with remote or no smoking history. Specifically, enrichment of EGFR and MET gene alterations were observed. These findings support the use of comprehensive molecular profiling in sqNSCLC. Furthermore, treatment outcomes demonstrate frequent objective responses and high clinical benefit rate supporting the use of targeted therapies in sqNSCLC harboring AGAs. This analysis provided rationale for further research of larger datasets investigating therapeutic approaches in sqNSCLC, which may have significant implications for consensus guideline recommendations and routine clinical practice.

cancer biology↗

Aging compromises Zebrafish caudal fin regeneration by disrupting Regenerative gene networks and Cellular metabolism

Zebrafish are widely recognized as a powerful vertebrate model for studying epimorphic regeneration due to their remarkable ability to restore complex tissues. However, regenerative efficiency declines with age, potentially due to alterations in gene regulatory networks and cellular metabolism. In the present study, we investigated the molecular and bioenergetic basis of age-associated regenerative decline by comparing young adult (<1 year) and old adult (>3 years) zebrafish during caudal fin regeneration. To further examine the contribution of mitochondrial function, mitochondrial dysfunction was experimentally induced using rotenone (20 nM), a mitochondrial Complex I inhibitor. Regenerative progression was assessed morphologically at 12hpa, 1dpa, 2dpa, 3dpa, and 7dpa, revealing a pronounced delay in fin regrowth in aged and rotenone-treated fish compared with young controls. Behavioral analysis indicated subtle but non-significant changes across experimental groups. Gene expression analysis using quantitative real-time PCR revealed age- and mitochondria-associated dysregulation of key regenerative gene families involved in developmental patterning, extracellular matrix organization, cellular signaling, and mitochondrial metabolism. Proteomic profiling further identified differential expression of proteins associated with mitochondrial bioenergetics, extracellular matrix remodeling, and signaling pathways required for blastema formation and tissue outgrowth. Ultrastructural examination by transmission electron microscopy revealed pronounced mitochondrial abnormalities, including enlarged mitochondria with fragmented or disrupted cristae, in aged and rotenone-treated regenerating tissues. Collectively, our integrative analysis establishes a mechanistic link between aging, mitochondrial dysfunction, and compromised regenerative capacity in zebrafish. The findings provide broader insights into metabolic constraints underlying age-related decline in regenerative potential in vertebrates.

developmental biology↗

A novel technique for monitoring Alzheimer's disease associated changes in brain-derived extracellular vesicle cargos in mouse models

Extracellular vesicles (EVs) are critical mediators of intercellular communication, carrying molecular cargos such as small noncoding RNAs (ncRNAs) that reflect the physiological and pathological state of their cells of origin. However, studying brain-derived EVs has been challenging due to the blood-brain barrier. Here, we optimized and validated an open-flow microdialysis (OFM) protocol for sampling EVs directly from brain interstitial fluid (ISF) in wild-type and APP/PS1 transgenic mice. Ex-vivo validation using plasma EVs demonstrated that OFM effectively captures the full EV population. In-vivo cerebral OFM (cOFM) enabled successful collection of brain ISF EVs, which were characterized by nanoparticle tracking analysis (NTA), electron microscopy, and western blotting, confirming their similarity to EVs isolated directly from brain tissue and plasma. Identification of small ncRNA cargos revealed that EVs sampled from brain ISF by cOFM were enriched in brain-specific signatures, many of which are associated with neuronal cell populations and biological functions. Furthermore, we observed a unique small ncRNA signature from the brain ISF EVs in the Alzheimers disease preclinical model compared to wild-type mice. These small ncRNAs were associated with genes considered important in biological functions associated with neurodegeneration. Our findings demonstrate that cOFM is a powerful tool for in-vivo sampling of brain EVs and highlight the unique molecular landscape of ISF EV small ncRNA cargos. This study offers new opportunities for biomarker discovery and mechanistic insights into neurodegenerative diseases, such as Alzheimers disease.

neuroscience↗

Rapid Cas13a-based penA genotyping for cefixime susceptibility in Neisseria gonorrhoeae

BackgroundAntimicrobial resistance in Neisseria gonorrhoeae is an urgent public health threat. Resistance-guided therapy can assure appropriate treatment and reintroduce alternative therapeutic options by identifying genetic predictors of resistance. Mosaicism at codons 375-377 of the penA gene are associated with cefixime resistance. Rapid, field-deployable assays for predicting cefixime susceptibility are lacking. MethodsWe used a machine-learning algorithm to develop a CRISPR Cas13a-based assay to detect the absence of mosaicism at codons 375-377 of the penA gene combined with isothermal amplification in a single reaction. We integrated the assay onto a portable fluorescence-based platform. We evaluated performance using cultured isolates and compared results with PCR genotyping and phenotypic antimicrobial susceptibility testing. We also assessed feasibility of reagent lyophilization for cold-chain-independent deployment. ResultsAmong 40 N. gonorrhoeae isolates, the Cas13a penA assay demonstrated 100% concordance with PCR genotyping and 92{middle dot}5% (95% CI 79.6-98.4%) concordance with phenotypic cefixime susceptibility. Median time to detection was 12 minutes (IQR 5 minutes). The lyophilized detection system detected all 12 isolates with a median time to detection of 45{middle dot}0 minutes (IQR 40-45) compared to 45{middle dot}0 minutes (IQR 35-50) for the positive aqueous control, although peak fluorescence was higher for the aqueous control (p<0.01). ConclusionThe Cas13a assay was rapid and demonstrated strong correlation with genotypic and phenotypic cefixime susceptibility in N. gonorrhoeae, while a lyophilized assay retained functionality.

bioengineering↗

Drift, selection and convergence in the evolution of a nonribosomal peptide

Nonribosomal peptides play important roles in microbial ecology and medicine, for example as toxins and antibiotics such as penicillin1. Like ordinary proteins, nonribosomal peptides are subject to evolutionary change, which is driven by rampant recombinations of their synthetases2. This makes it difficult to study the evolutionary histories of nonribosomal peptides, because recombination is a serious challenge for phylogenetic inference3. Here we use recombination-aware phylogenetics and ancestral sequence reconstruction to retrace the evolution of GameXPeptides, nonribosomal peptides entomopathogenic bacteria use to kill their insect prey4. By untangling the complex histories of their synthetases, we discover dozens of new GameXPeptides and show striking patterns of structural convergence. In analogy to classic statistical test for natural selection acting on nucleotide mutations, we develop a similar test for whether selection acts to fix recombinations. We provide statistical and experimental evidence of both neutral genetic drift and natural selection in the diversification of GameXPeptides. GameXPeptides variants rapidly evolved highly insect specific toxicities, suggesting that their diversification may be driven by an evolutionary arms race. Our work suggests that small, fast evolving alteration to nonribosomal peptides can overcome host resistance on short timescales, with important implications for the evolution of resistance evading antibiotics.

evolutionary biology↗

Strong STMP-Crosslinked Lignin/Chitosan Hydrogel Films with Enhanced Aqueous Stability and Bioactivity for Active Food Packaging

Plastic pollution has intensified globally due to the widespread use of non-biodegradable packaging materials. Conventional passive plastics used in food packaging lack adaptive functionality limiting their preservation efficiency. Biopolymer-based hydrogels offer promise due to their biodegradability, film-forming ability, and intrinsic bioactivity. However, their instability in aqueous environments constrains their application in high-moisture foods such as meat. Lignin extracted from sugarcane tops via acid-alkali treatment and chitosan known for its film-forming and antimicrobial properties were combined to enhance the antioxidant, antimicrobial, UV-blocking, and mechanical performance of the hydrogel. The films were cured at 25 {degrees}C under 80% relative humidity, eliminating the high temperature pre-oven drying required in conventional methods. Further, a stable lignin/chitosan hydrogel film was developed using sodium trimetaphosphate (STMP) as a crosslinker and glycerol as a plasticizer. The films treated with 1% (w/v) STMP for 15 min showed optimal performance, exhibiting 89.89% radical scavenging activity, complete UV shielding, antimicrobial activity against E. coli, and tensile strength of 2364.79 MPa with 31.49% elongation at break. The film retained its integrity in food simulants namely ethanol (10% v/v), acetic acid (3% v/v), and distilled water. In chicken breast packaging trials, the CL-0.8/3Cht film-maintained pH, moisture, and protein stability and significantly reduced microbial load during 5 days of storage. These findings establish the CL-0.8Lig/3Cht hydrogel film with agri-residue derived lignin as a robust, multifunctional, and biodegradable active packaging material for moisture-rich food systems. These findings support waste valorisation advancing cleaner and sustainable food preservation practices.

bioengineering↗

AlveolEye: Rapid and precise lung morphometry guided by computer vision

Rigorous and reproducible evaluation of lung tissue under different conditions is necessary to interpret development, injury, and pharmacologic interventions. Common histological measurements in the distal lung include mean linear intercept (MLI) as a metric of alveolarization and airspace volume density (ASVD) as a metric of airspaces relative to tissue. Historically, these have been performed manually in a time-intensive process, with reproducible trends, but a high degree of variability between individuals. To improve the reproducibility and throughput of lung morphometry, we developed AlveolEye, an open source, semi-automated, computer vision-assisted tool that rapidly and reproducibly calculates MLI and ASVD from images of standard hematoxylin and eosin (H&E) stained tissue sections. AlveolEye-assisted MLI calculation closely aligns with manually-derived measurements for corresponding images, with preservation of trends in measurements between non-injured controls and neonatal mice subjected to two different injury models. Analyzing human tissue of varying ages suggests that the approach developed in AlveolEye is generalizable across species. Notably, AlveolEye markedly reduced the average variation across individual analyzers, with the greatest improvement in precision among individuals with the least experience in performing lung morphometry. The design of AlveolEye is intentionally semi-automated, preserving the investigators ability to assess and adjust parameters based on sample characteristics. AlveolEye facilitates efficient lung morphological measurements on larger sample sizes, allowing for greater statistical power for preclinical studies, and improves precision across individual observers, allowing for improved rigor in experimental design and execution.

developmental biology↗

Functional connectivity reveals increased network segregation and sensorimotor processing during working memory in adolescents with Neurofibromatosis Type 1

Neurofibromatosis type 1 (NF1) is a rare, monogenic condition associated with impairments in working memory processing. However, it is unknown to what extent these impairments are explained by disrupted connectivity and state transitions of the functional brain networks. This study characterised task-state functional connectivity (FC) and network controllability during working memory in NF1 and investigated whether altered controllability distinguished NF1 from neurotypical controls and related to individual differences in working memory performance. We analysed functional MRI data from 53 NF1 adolescents and 36 age-matched neurotypical controls performing a verbal N-back task. Compared to controls, NF1 participants showed reduced FC within frontoparietal network (particularly between the left prefrontal cortex and left intraparietal sulcus), reduced FC between default and limbic networks, and increased FC between control and somatomotor regions. Network controllability analysis revealed increased average controllability but reduced modal controllability and activation energy in prefrontal, parietal, temporal and retrosplenial regions in NF1, indicating that in NF1 these regions have enhanced capacity to drive the network toward easy-to-reach states and are readily activated within the current network organisation. The opposite pattern of reduced average controllability but increased modal controllability and activation energy were observed in somatosensory, auditory, extrastriate and temporal-parietal regions, suggesting enhanced capacity of these regions to drive the network towards difficult-to-reach states. These changes accurately predicted NF1 status, with an area under the ROC curve exceeding 80% across all controllability models. Furthermore, average controllability accurately predicted working memory performance in the NF1 group, generalising to out-of-sample data. In particular, left and right lateral ventral prefrontal cortex, left superior parietal lobule, left intraparietal sulcus consistently emerged as predictors of working memory performance across all measures. By demonstrating that altered regional network controllability in NF1 predicts working memory performance, this study provides a novel mechanistic account of the functional network alterations underlying cognitive difficulties in NF1 and establishes a framework for evaluating future therapeutic interventions through their effects on functional brain network control.

neuroscience↗

Repetitive magnetic stimulation with iTBS600 induces persistent structural and functional plasticity in mouse organotypic slice cultures

BackgroundRepetitive transcranial magnetic stimulation (rTMS) is well known for its ability to induce synaptic plasticity, yet its impact on structural and functional remodeling within stimulated networks remains unclear. This study investigates the cellular and network-level mechanisms of rTMS-induced plasticity using a clinically approved 600-pulse intermittent theta burst stimulation (iTBS600) protocol applied to organotypic brain tissue cultures. MethodsWe applied iTBS600 to entorhino-hippocampal organotypic tissue cultures and conducted a 24-hour analysis using c-Fos immunostaining, whole-cell patch-clamp recordings, time-lapse imaging of dendritic spines, and calcium imaging. ResultsWe observed long-term potentiation (LTP) of excitatory synapses in dentate granule cells, characterized by increased mEPSC frequencies and spine remodeling over time. c-Fos expression in the dentate gyrus was transient and exhibited a clear sensitivity to the orientation of the induced electric field, suggesting a direction-dependent induction of plasticity. Structural remodeling of dendritic spines was temporally linked to enhanced synaptic strength, while spontaneous firing rates remained stable during the early phase in the dentate gyrus, indicating the engagement of homeostatic mechanisms. Despite the widespread electric field generated by rTMS, its effects were spatially and temporally precise, driving Hebbian plasticity and region-specific spine dynamics. ConclusionsThese findings provide mechanistic insights into how rTMS-induced LTP promotes targeted plasticity while preserving network stability. Understanding these interactions may help refine stimulation protocols to optimize therapeutic outcomes.

neuroscience↗

Evaluation of Immunopharmacological Efficacy of Live Leishmania donovani Overexpressing Ld_ζ1domain for Protection Against Experimental Human Visceral Leishmaniasis

ObjectiveTo evaluate the efficacy and immunogenicity of the zeta domain over-expressing Leishmania donovani (Ld_{zeta}1domain) as a vaccination candidate against visceral leishmaniasis (VL). MethodsIn this study, Leishmania overexpressor Ld_{zeta}1domain (OE) were transformed by electroporation using a GFP-tagged Ld_{zeta}1domain recombinant plasmid. The resulting overexpressing cells were analysed in vitro to assess their growth dynamics and infectivity. We also investigated the immune-protective potential of these overexpressor in a mouse model challenged with Leishmania donovani. The immune response, including Th1 and Th2 pathways, was thoroughly characterized using RT-PCR and ELISA assays. In addition, the study conducted a thorough evaluation of the mouses spleen and liver parasites, as well as quantitative evaluation of tissue pathological changes. ResultsLd_{zeta}1 domain (OE) parasites exhibited significantly lower viability and replication rates than WT parasites, and in vivo studies showed that mice immunized with the Ld_{zeta}1(OE) domain had lower parasite numbers than mice infected with LdWT. Spleen and liver showed significant histological changes suggestive of protection. Parasite burden in the spleen and liver of vaccinated mice were significantly reduced. The immune response showed increased IFN-{gamma} levels and lower IL-10 production, resulting in a greater IFN-{gamma}/IL-10 ratio, indicating parasite elimination. The vaccination also caused a significant IgG humoral response and increased nitric oxide production in immunized mice. ConclusionOur findings demonstrated that overexpressing the zeta toxin resulted in controlled parasite attenuation, lowering pathogenicity while retaining immunogenic features. Our work established the zeta over-expressors protective efficacy, immunogenicity, and proliferation in response to a Leishmania challenge in vitro and in vivo. This preliminary prototype study suggested that Ld_{zeta}1domain (OE) parasites may be suitable for developing an attenuated vaccine against leishmaniasis. Graphical representation O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=88 SRC="FIGDIR/small/630021v1_ufig1.gif" ALT="Figure 1"> View larger version (18K): org.highwire.dtl.DTLVardef@32dfc0org.highwire.dtl.DTLVardef@1ffe89dorg.highwire.dtl.DTLVardef@d9feorg.highwire.dtl.DTLVardef@1e7bae7_HPS_FORMAT_FIGEXP M_FIG C_FIG A schematic representation on the protective effectiveness, immunogenicity, and proliferation of the zeta over-expressor in response to Leishmania challenge in vitro and in vivo model.

pathology↗

The CD4 T cell-independent IgG response during persistent virus infection favors emergence of neutralization-escape variants

How changes in the quality of anti-viral antibody (Ab) responses due to pre-existing or acquired CD4 T cell insufficiency affect virus evolution during persistent infection are unknown. Using mouse polyomavirus (MuPyV), we found that CD4 T cell depletion before infection results in short-lived plasma cells secreting low-avidity antiviral IgG with limited BCR diversity and weak virus-neutralizing ability. CD4 T cell deficiency during persistent infection incurs a shift from a T-dependent (TD) to T-independent (TI) Ab response, resembling the pre-existing TI Ab response. CD4 T cell loss before infection or during persistent infection is conducive for emergence of Ab-escape variants. Cryo-EM reconstruction of complexes of MuPyV virions with polyclonal IgG directly from infected mice with pre-existing or acquired CD4 T cell deficiency enabled visualization of shortfalls in TI IgG binding. By debilitating the antiviral IgG response, CD4 T cell deficiency sets the stage for outgrowth of variant viruses resistant to neutralization. ONE SENTENCE SUMMARYPre-existing and acquired CD4 T cell deficiency facilitates outgrowth of Ab-escape viral variants during persistent infection.

immunology↗

Erythrocytic plasma membrane calcium ATPase (PMCA4b) variations mediate redox imbalance to determine artemisinin sensitivity in malaria

Artemisinin resistance in Plasmodium falciparum remains a major public health challenge for the ongoing malaria elimination programs. Till now, artemisinin resistance is linked with the variations in the genome of P. falciparum which are mainly clustered in the Pfkelch13 gene. Several studies reported artemisinin resistance in the malaria endemic areas without finding any evidence of genetic variation in parasite for this occurrence. This study interrogated whether host genetic variations have any association with artemisinin sensitivity of malaria parasite. We investigated the relationship of 1) genetic variations in the human ATP2B4 gene and 2) the resultant surface expression of plasma membrane calcium ATPase (PMCA4b) with the intraerythrocytic levels of calcium, reactive oxygen species (ROS) and the resistance towards artemisinin in the intraerythrocytic parasite. This study found negative correlation of PMCA4b expression level with intraerythrocytic calcium and ROS levels. Further in-vitro growth assays revealed that artemisinin sensitivity is reduced in the parasites growing within the RBCs having low PMCA4b and high oxidative stress. Overall, this study highlights the strong association of host PMCA4b in cellular calcium mediated redox imbalance, which significantly contributes to artemisinin resistance in malaria parasite. Hence, this is the first study to document the effect of host variations on artemisinin sensitivity of the parasite. We further emphasize that many redox modulating RBC polymorphisms that are prevalent in malaria endemic areas could influence artemisinin resistance and can serve as potential biomarkers for predicting therapeutic response. Thus, detailed population specific research may provide new insights for personalized malaria treatment and may inform future drug development strategies. SignificanceThe human host and malaria parasite share a closely interconnected relationship hence host variations could influence parasite drug resistance. This study demonstrates that reduced PMCA4b expression, the primary calcium efflux pump in RBCs, significantly increases the erythrocytic calcium and reactive oxygen species (ROS) levels, thereby decreasing the P. falciparum growth as well as artemisinin sensitivity. Many ROS inducing RBC polymorphisms, such as sickle cell, thalassemia, G6PD deficiency, PMCA4b variations etc. have emerged as strong malaria protective traits in several studies in malaria endemic areas. But these traits could also influence artemisinin resistance and can serve as potential biomarkers for predicting therapeutic response and highlights the importance of host erythrocytes oxidative microenvironment surveillance in monitoring antimalarial drug resistance.

microbiology↗

Development of a Novel Hybprinter-SAM for Functionally Graded Tissue Engineering Constructs with Patterned and Localized Biochemical Signals

Engineering native-mimetic tissue constructs is challenging due to their intricate biological and structural gradients. To address this, Hybprinter-SAM was developed by integrating three bioprinting technologies: syringe extrusion (SE), acoustic droplet ejection (ADE) and molten material extrusion (MME). This system enables not only the creation of mechanical gradients by combining soft and rigid materials but also precise patterning and controlled localization of biochemical signals within printed scaffolds. This capability is beneficial in replicating the complexity of native tissues to enhance functionality. Both the printing process and biomaterials were optimized to balance printability, mechanical integrity, and biocompatibility. As a proof of concept, Hybprinter-SAM was used in a bone-tendon regeneration study to engineer a multi-material construct with patterned fibroblast growth factor 2 (FGF-2), resulting in markers indicative of fibrocartilage development. These findings highlight the potential of Hybprinter-SAM as a versatile platform for diverse tissue engineering applications that require complex, functionally graded tissue constructs.

bioengineering↗

Effects of non-invasive brain stimulation on effective connectivity during working memory task in Neurofibromatosis Type 1 patients

This study examined the effects of anodal transcranial direct current stimulation (atDCS) on effective connectivity during a working memory task. Eighteen adolescents with Neurofibromatosis Type 1 (NF1) completed a single{square}blind sham{square}controlled cross{square}over randomised atDCS trial. Dynamic causal modelling was used to estimate the effective connectivity between regions that showed working memory effects from the fMRI. Group-level inferences for between sessions (pre- and post-stimulation) and stimulation type (atDCS and sham) effects were carried out using the parametric empirical Bayes approach. A correlation analysis was performed to relate the estimated effective connectivity parameters of left dlPFC pre-atDCS and post-atDCS to the concentration of gamma-aminobutyric acid (GABA) measured via magnetic resonance spectroscopy (MRS-GABA). Next, correlation analysis was repeated using all working memory performance and all pre-atDCS and post-atDCS connectivity parameters. It was found that atDCS decreased average excitatory connectivity from left dorsolateral prefrontal cortex (dlPFC) to left superior frontal gyrus and increased average excitatory connectivity to left globus pallidus. Further, reduced average intrinsic (inhibitory) connectivity of left dlPFC was associated with lower MRS-GABA. However, none of the connectivity parameters of dlPFC showed any association with performance on a working memory task. These findings suggest that atDCS reorganised connectivity from frontal to fronto-striatal connectivity. As atDCS-related changes were not specific to the effect of working memory, they may have impacted general cognitive control processes. In addition, by reducing MRS-GABA, atDCS might make dlPFC more sensitive and responsive to external stimulation, such as performance of cognitive tasks. Highlights- atDCS was applied to left dlPFC in NF1 patients during working memory - After atDCS, no effect on modulatory connectivity - Evidence for increased N-back average connectivity from dlPFC to globus pallidus - Less dlPFC MRS-GABA was associated with less dlPFC inhibition

neuroscience↗

Bronchopulmonary Dysplasia with Pulmonary Hypertension Associates with Loss of Semaphorin Signaling and Functional Decrease in FOXF1 Expression

Lung injury in preterm infants leads to structural and functional respiratory deficits, with a risk for bronchopulmonary dysplasia (BPD) that in its most severe form is accompanied by pulmonary hypertension (PH). To examine cellular and molecular dynamics driving evolving BPD in humans, we performed single-cell RNA sequencing of preterm infant lungs in early stages of BPD and BPD+PH compared to term infants. Analysis of the endothelium revealed a unique aberrant capillary cell-state primarily in BPD+PH marked by ANKRD1 expression. Predictive signaling analysis identified deficits in the semaphorin guidance-cue signaling pathway and decreased expression of pro-angiogenic transcription factor FOXF1 within the alveolar parenchyma in neonatal lung samples with BPD/BPD+PH. Loss of semaphorin signaling was replicated in a murine BPD model and in humans with alveolar capillary dysplasia (ACDMPV), suggesting a mechanistic link between the developmental programs underlying BPD and ACDMPV and a critical role for semaphorin signaling in normal lung development.

genomics↗