Search bioRxiv⌕ Search

Biology subjects

Kaur, J.

Publications and source records attributed to Kaur, J..

At least 19 recordsLinked to original sources

A Dynamics-Informed Machine Learning Framework for Inhibitor Optimization Against Quickly Evolving Targets to Avoid Resistance

Drug resistance often emerges through mutations that reshape protein conformational ensembles, allowing inhibitor potency to be altered without directly disrupting protein-ligand contacts. Consequently, the molecular mechanisms underlying these effects remain difficult to identify, hindering the design of inhibitors with durable potency against rapidly evolving drug targets. To address this challenge, we developed ROBUST, a physics-informed machine learning framework that integrates experimental measurements, molecular dynamics simulations, and interpretable statistical modeling to identify energetic determinants of inhibitor potency. Using HIV-1 protease as a stringent model system for drug resistance, we determined 157 new inhibition constants and integrated them with prior measurements to establish a comprehensive experimental dataset of 364 protease-inhibitor pairs. Analysis of the corresponding molecular dynamics simulations revealed a compact network of energetic interactions that quantitatively explains how resistance mutations and inhibitor modifications jointly reshape molecular recognition and inhibitor potency across the multidimensional resistance landscape. Models constructed from these energetic signatures predicted binding free energies with high accuracy (RMSE < 1 kcal mol-1) and successfully generalized to unseen darunavir analogs. Importantly, ROBUST accurately prioritized unseen analogs based on their potency across the variant set, demonstrating its utility for identifying compounds with improved resistance profiles. Together, these results uncover the energetic principles through which resistance mutations and inhibitor modifications alter potency and establish ROBUST as a mechanistically interpretable framework for translating these insights into resistance-aware inhibitor optimization against rapidly evolving drug targets.

biophysics↗

Multimodal imaging maps spinal glymphatic transport in health and its disruption after injury

Spinal cord injury (SCI) is an incurable neurological condition in which post-traumatic edema contributes to secondary ischemic damage because the spinal cord is confined within the rigid vertebral canal. However, glymphatic transport in the healthy and injured spinal cord remains poorly characterized. We hypothesized that spinal cerebrospinal (CSF) and glymphatic transport is shaped by anatomy, administration route, and molecular size of the tracer; is disrupted after SCI; and is further impaired by loss of aquaporin-4 (AQP4). CSF tracers were administered by cisterna magna or lumbar intrathecal injection to anesthetized adult C57BL/6 mice. Dynamic contrast-enhanced MRI, ex vivo fluorescence imaging, and histology were used to characterize tracer distribution, influx, and clearance. Constrictions of the spinal subarachnoid space at C3-C7, T6-T12 and L5-S1 spinal segments accelerated contrast-agent dispersion, demonstrating that local anatomy regulates spinal CSF transport. Tracer influx into the cord itself occurred primarily along periarterial pathways.Tracer distribution depended on the administration route: cisterna magna injection preferentially labeled white matter in the upper spinal cord, whereas lumbar injection preferentially labeled grey matter in the lower spinal cord. Gadobutrol and ovalbumin penetrated and dispersed throughout the parenchyma, whereas fibrinogen remained confined to the meninges. Under physiological conditions, intraparenchymal tracers cleared within 24 h. SCI was modeled using a minimally invasive NMDA-induced lesion at T11 that produced focal necrosis while preserving the dura and vertebral structures. Glymphatic transport, lesion volume, and motor recovery were compared between wild-type and AQP4-knockout mice using imaging, the Basso Mouse Scale, and voluntary wheel running. After SCI, intrathecal contrast propagated more rapidly, especially at T7-T8 segments and at the S1 segment, but tissue clearance was profoundly impaired, with tracer retention persisting for up to seven days. AQP4-knockout mice showed greater clearance impairment, larger lesions, and poorer motor recovery than wild-type controls compared at 24 h. These findings define major determinants of spinal glymphatic transport and show that accelerated tracer propagation after SCI does not indicate effective clearance. Instead, SCI produces glymphatic dysfunction that is exacerbated by loss of AQP4 and associated with greater tissue damage and functional impairment. The results extend the glymphatic framework to the spinal cord and identify fluid-clearance pathways as potential therapeutic targets for limiting edema and secondary injury. Future studies should determine whether restoring glymphatic function improves neurological recovery after SCI.

neuroscience↗

Integrated miRNA-protein profiling of small extracellular vesicle cargo reveals dynamic cargo remodelling during tissue repair in UV-C-damaged C. elegans

Ultraviolet-C (UV-C) radiation is a potent environmental stressor that induces DNA damage, accumulation of reactive oxygen species (ROS), and cellular dysfunction. This also initiates coordinated molecular responses to regulate cellular adaptation and recovery. Small extracellular vesicles (sEVs) have emerged as key mediators of intercellular communication through the selective incorporation of microRNAs (miRNAs), proteins, and lipids. However, the temporal changes of sEV-associated cargo during the progression from UV-C-induced damage to recovery remain uncharacterized. We hypothesised that UV-C exposure induces stage-specific changes in sEV cargo (miRNA and proteins) that promote the transition of cells from damage to the response and recovery phases. To examine this, a time-resolved UV-C exposure model was established using Caenorhabditis elegans (C. elegans). In this paper, we studied 2.5 hours of UV-C exposure, including cellular damage, intracellular ROS levels, and DNA integrity, to define the damage and repair state. Based on these temporal variations, samples were collected: i) immediately after exposure, ii) 6 hours post-exposure, and iii) 16 hours post-exposure were designated as damage, response, and recovery conditions, respectively. sEVs isolated from whole-worm preparations were characterised using biophysical and molecular approaches, followed by miRNA sequencing and proteomic analyses. Integrative analysis further identified miRNA-protein associations and associated them with pathways involved in stress adaptation, metabolism, signal transduction, and cellular homeostasis. Collectively, these findings provide a temporal molecular framework of sEV cargo associated with UV-C-induced damage, response, and recovery in C. elegans. Overall, this study identified candidate molecular signatures and miRNA-protein associations that underlie the temporally selective packaging of sEV-associated cargo following UV-C-induced damage, providing a basis for future tissue-specific and mechanistic investigations.

molecular biology↗

Estrogen is Coupled to the Calcium Release Machinery in HumanLeiomyoma Cells

Uterine leiomyomas, commonly known as fibroids, are benign tumors of the female reproductive tract. They are the most common tumor of the female reproductive system and the leading cause of hysterectomy in the United States. Progesterone, estrogen, and their receptors are important drivers for the development and growth of leiomyomas. How estrogen drives leiomyoma growth remains unclear. We have previously shown that simvastatin can inhibit leiomyoma growth by modulating intracellular calcium. This suggests that calcium signaling is important for leiomyoma growth. We therefore hypothesized that estrogen may drive leiomyoma growth by stimulating calcium release through the membrane estrogen receptor GPR30 (also known as GPER). We found that estrogen dose-dependently induced calcium release in leiomyoma cells. The GPR30-specific agonist G-1 also induced calcium release, indicating that GPR30 mediates estrogen-mediated calcium release. The GPR30 antagonist G-15 blocked estrogen-induced calcium release and significantly reduced leiomyoma proliferation. Our results demonstrate that GPR30 is a major driver of estrogen-dependent growth in leiomyoma cells by modulating intracellular calcium. These findings may have high therapeutic relevance to leiomyomas and other estrogen-dependent tumors.

cell biology↗

Efficacy of 60 personal mosquito repellents and perfumes against Aedes aegypti mosquitoes

Personal insect repellents can offer an effective means of preventing mosquito bites. Despite a wide variety of products that claim to repel mosquitoes, relatively few studies have systematically compared their performance through standardized tests. In Australia, chemical-based repellents must be registered with the Australian Pesticides and Veterinary Medicines Authority (APVMA); however, many unregistered products with unverified effectiveness remain commercially available. Here, we tested 55 insect repellents and 5 non-repellent perfumes and deodorants sold in Australia for their protection against Aedes aegypti mosquito landings (as a proxy for bites) using arm-in-cage assays across eight human subjects. We tested 43 topical repellents (containing 18 different primary active ingredients), four wristbands, three clothing stickers, three ultrasonic devices, one garment, one repellent applied to fabric, two perfumes, two deodorants and one antiperspirant. Thirteen repellents, including all wristbands, stickers and ultrasonic devices did not provide complete protection against mosquito landings for any human subject, while a further sixteen provided complete protection for 1 hr or less on average. Repellents containing DEET, oil of lemon eucalyptus, picaridin and IR3535 as the primary active ingredient were the only products that provided more than 2 hours of complete protection, but with significant variation among products with the same active ingredient. Only 7/30 essential oil-based topical repellents and perfumes provided complete protection for greater than 1 hr. Nearly half (25/52) of the repellents subject to registration with the APVMA were unregistered despite being advertised or labelled as mosquito repellents, and these tended to be less effective than registered products. Only 5/28 repellents met or exceeded their claimed protection time. This study highlights the prevalence of unregistered and ineffective mosquito repellents on the Australian market while providing evidence for products and active ingredients that do protect against mosquito bites under laboratory conditions.

zoology↗

Beyond pain: a brain-based biomarker predicts individual pain relief

Effective pain relief is a central goal of medical care, yet objective biomarkers of pain relief are lacking. Using task-based functional MRI and a capsaicin-induced tonic heat pain model, we experimentally elicited both pain exacerbation and pain relief within the same individuals. Existing brain-based signatures, including the Neurologic Pain Signature (NPS), reliably detected pain increases, but failed to capture pain relief. We therefore developed the PAin and RElief Signature (PARES), a multivariate brain signature trained to predict bidirectional changes in pain perception in n = 61 healthy controls. PARES robustly predicted both pain increases and relief and generalized to an independent cohort of people with chronic back pain (n = 58), who underwent the same experimental procedures. Together these findings establish a neural signature of pain relief and provide a potential biomarker for treatment stratification and analgesic development.

neuroscience↗

Conformational selection drives substrate-ATP coupling in the type VI ABC transporter

The mechanism of substrate-ATP coupling is central to the function of ABC transporters. Substrates bind to the specialized transmembrane domains (TMDs), whereas ATP binding and hydrolysis occur in the conserved intracellular nucleotide-binding domains (NBDs). Efficient substrate transport requires coupling between these processes, in which the intracellular coupling helices play an essential role. Here, we probed both coupling helices of the type VI ABC transporter LptB2FG(C), the core complex responsible for intermembrane lipopolysaccharide (LPS) transport in Gram-negative bacteria, using site-specific 19F labeling and ultra-fast MAS NMR. We show that both coupling helices exist in an equilibrium among three major conformational states. Progression through the coupling cycle occurs via conformational selection, as LPS and nucleotide binding shift the conformational equilibrium, providing evidence for bidirectional communication between the TMDs and NBDs. Furthermore, the conformational distributions of the two coupling helices are asymmetric. Finally, complex formation with LptC, a unique feature of type VI ABC transporters, symmetrizes the conformational landscape of the coupling helices and facilitates transitions between conformational states, thereby enhancing the efficiency of coupling ATP hydrolysis to LPS transport. Together, our findings establish the coupling helices as dynamic allosteric elements that integrate nucleotide and substrate binding through conformational selection, providing a mechanistic framework for substrate-ATP coupling in ABC transporters.

biophysics↗

Neural fiber orientations across spinal cord gray matter

Understanding connectivity within the nervous system is central to understanding its function, and the network architecture of many brain regions has been mapped in fine detail. The sub-tract organization of neuronal projections within the human cord, particularly in gray matter is essentially unknown. Since full connectomic reconstruction is currently intractable at this scale, a tractable first step is to statistically characterize neurite orientations across spinal regions. Here we combine a ~400 hour 9.4T ex vivo high-angular-resolution diffusion-weighted MRI spanning all segments (C1-S5) of a post-mortem human spinal cord with structure-tensor analysis of SMI-32 neurofilament fluorescence microscopy to map neurite orientation across the cord. We find that projection geometry varies systematically along the rostro-caudal axis. Cervical, lumbar, and sacral gray matter exhibit low anisotropy, high orientation dispersion, and predominantly transverse fiber populations (>91% of orientations), consistent with dense segment-local circuitry. Thoracic gray matter is categorically distinct from the rest of the cord with elevated axial diffusivity, white-matter-like anisotropy, and a fiber orientation distribution in which 60% of orientations run within a polar angle of 85-95{degrees} i.e., along the the cord's rostro-caudal axis. Micron-resolution microscopy independently supports this longitudinal architecture. Together, these findings reveal a regional dissociation in spinal gray-matter wiring and suggest a coupling between projection geometry and the distinct processing demands of each segment.

neuroscience↗

Occurrence of Biased mTOR Signaling in Hepatocellular Carcinoma

BackgroundmTOR signaling promotes cell growth and anabolic processes in all eukaryotes. Hyperactivation of mTOR signaling is associated with various cancers along with hepatocellular carcinoma (HCC). HCC is a highly lethal malignancy with multiple aetiologies such as viral infection, alcohol abuse, and metabolic dysfunction. Therapeutic options for HCC remain limited due to an incomplete understanding of oncogenic drivers and poorly characterized mechanisms of disease progression. MethodsVarious regimens of DEN and CCl4 carcinogen dosage were investigated on C57BL/6J mice to induce HCC. The histological analysis for fibrosis and serum markers for liver function were performed. Molecular analyses of oncogenic drivers were performed in the HCC tissues obtained from mice and HCC patients. The impact of inhibition of mTOR signaling was assessed on HCC progression. ResultsWe established a rapid DEN+CCl4 induced (DCI) HCC model in C57BL/6 mice to study disease progression longitudinally. The molecular analysis revealed upregulation of MAPK and downregulation of mTORC1-S6K-S6 signaling in HCC. However, other branches of mTOR such as mTORC1-ULK1, mTORC1-4EBP1, and mTORC2-PKC were upregulated due to the increased expression. Similar observations were found in tissues derived from HCC patients. Furthermore, inhibition of mTORC1 alone by Rapamycin did not reduce HCC progression but Torin 1 mediated inhibition of both mTORC1 and mTORC2 significantly reduced HCC progression. ConclusionsWe propose this biased mTOR signaling modulates mTOR activity towards specific downstream processes that are crucial for cancer cell growth and targeting both the mTOR complexes has better therapeutic potential in HCC. Impact and ImplicationsThis study provides a rapid pre-clinical model for understanding HCC progression and to explore various intervention strategies. The study reports a novel phenomenon of biased mTOR signaling where deregulation of downstream substrate levels modulates the mTOR activity towards the specific branches, the master regulator of cell growth and metabolism. Furthermore, the study suggests that the clinical investigations exploring the rapalogs against HCC should be cautiously considered depending on the aetiology and signaling status of HCC. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=125 SRC="FIGDIR/small/727188v2_ufig1.gif" ALT="Figure 1"> View larger version (20K): org.highwire.dtl.DTLVardef@ef3714org.highwire.dtl.DTLVardef@1091b25org.highwire.dtl.DTLVardef@d52f2forg.highwire.dtl.DTLVardef@cc158_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIDEN and CCl4 treatment generated a well-established HCC within 4 months. C_LIO_LILiver fibrosis and serum markers correlated with HCC progression. C_LIO_LIUpregulation of mTOR pathway substrates create biased mTOR signaling. C_LIO_LIDual inhibition of mTORC1 and mTORC2 reduced HCC progression significantly. C_LI

cancer biology↗

Revisiting the diversity of secondary endosymbionts in the major pest oat aphid, Rhopalosiphum padi

There is disagreement on whether secondary endosymbionts are found in the major cereal pest aphid, Rhopalosiphum padi. Some papers report a diversity of secondary bacterial endosymbionts while others have failed to find evidence of these bacteria in this species. Here we revisit this issue by summarizing the relevant literature and through additional sampling of the species in Australia, China and Denmark using a combination of molecular approaches. We find a general absence of secondary endosymbionts beyond the obligate endosymbiont Hamiltonella defensa in R. padi. While the inconsistency in survey results may reflect rapid changes in endosymbiont turnover in populations and/or the impact of ecological factors such as host plant type on endosymbiont diversity, we are concerned that technical issues may be at least partly responsible for inconsistencies in the literature. This leads us to emphasize the importance of multiple sources of evidence required to establish and characterize endosymbiont infections, including PCR and qPCR assays, DNA Sanger sequencing and 16SrRNA gene metabarcoding. We note that several major aphid pests show a low incidence of secondary endosymbionts which raises issues about the importance of these endosymbionts in aphids that constitute pests, even though endosymbionts can in some cases increase host fitness and therefore pest impact.

microbiology↗

Comparative Analysis of Structural and Dynamical Properties of Lipid Membranes Simulated with the AMBER Lipid21 ForceField Using SPC/E, TIP3P, TIP3P-FB, TIP4P-FB, TIP4P-Ew, TIP4P/2005, TIP4P-D, and OPC Water Models

We have conducted all atom molecular dynamics simulations of POPC and DPPC lipid bilayers using AMBER Lipid21 force field with eight different water models, including SPC/E, TIP3P, TIP3P-FB, TIP4P-FB, TIP4P-Ew, TIP4P/2005, TIP4P-D, and OPC, to identify the most compatible one without any modification. A number of parameters have been computed in order to understand the structure of the lipid bilayer: Area per lipid, Isothermal compressibility modulus, average Volume per lipid, electron density profile, bilayer thickness, X-ray and neutron scattering form factors, deuterium order parameter, and radial distribution function. The estimated Area per lipid, Isothermal compressibility factor, volume per lipid and bilayer thickness are highly consistent with experimental results for the SPC/E water model, indicating its suitability with the AMBER Lipid21 force field, insted of any modification. The bilayer electron density profiles of both the lipid bilayers demonstrate a little augmentation of water penetration with respect to the membrane surface for TIP4P-D water model. However, the experimental X-ray and neutron scattering form factors are aligning well with the simulated results for all studied water models, and TIP4P-D shows better for X-ray data. The deuterium order parameter for lipid acyl chains value less than 0.25 for all observed water models, depicting their disorderness for both the lipid bilayers. The lateral diffusion and reorientation autocorrelation function of the lipid molecules in both the bilayers are computed to reveal their dynamics across all water models. In comparison to other water models, the simulated trajectories predict better structure and reasonably fair dynamic properties for the SPC/E water model. The TIP4P-Ew water model reproduces the lateral diffusion co-efficient in close agreement with experiment. Reorientational dynamics for both the lipids in the bilayers for eight different water models are observed; the presence of slow and slowest time components corresponds to the lipid axial motion (wobble motion) and Twist/Splay motions. So, in view of the overall performance of the different water models with the AMBER Lipid21 all atom force field in reproducing membrane physical properties, the SPC/E water model appears to be an optimal choice.

bioinformatics↗

Laboratory and wild Drosophila sechellia have conserved niche specialization phenotypes

A major challenge to investigating the proximate causes of ecological adaptation is the difficulty of studying the phenotypes of organisms in their natural environments. By necessity, many studies seeking to determine the genetic and cellular basis of adaptation therefore investigate potentially adaptive phenotypes under laboratory conditions where organisms are more easily experimentally manipulated. For laboratory models, it remains unclear if organisms maintained long term under laboratory conditions are representative of relatives in their natural environment. In recent years, Drosophila sechellia, a specialist species endemic to the Seychelles, has emerged as a (neuro)genetic model for studying the molecular basis of ecological adaptation. A multitude of studies have investigated the genetic and cellular basis of various aspects of this species specialization in a laboratory setting. However, the vast majority of these studies use laboratory strains of D. sechellia that were collected many decades ago, and have been maintained under conditions very different from their natural niche. Thus, it remains unclear if and how these strains resemble their wild counterparts. Here, we compare the phenotypes of these laboratory strains with recently-collected wild D. sechellia to ask if laboratory strains display a loss or degradation of phenotypes potentially involved in their specialization resulting from their long-term laboratory maintenance. Across several behavioral and anatomical phenotypes, we find a high degree of similarity between wild-caught and laboratory-maintained strains. Our results suggest that studies of the molecular mechanisms underlying D. sechellias phenotypes associated with specialization are likely representative of the evolution of these flies in the wild.

evolutionary biology↗

Cell State Chaos Underpins the Evolution of SMARCA4-Deficient Dedifferentiated Endometrial Cancer

Dedifferentiated endometrial carcinoma (DDEC) is a histologically unique cancer type, wherein well-differentiated regions lie adjacent to morphologically distinct, high-grade lesions that are histologically undifferentiated. Previous studies have determined that in nearly half of the cases dedifferentiation is associated with the genomic inactivation of SMARCA4, a catalytic subunit belonging to the SWI/SNF chromatin remodelling complex (SWI/SNF CRC), suggesting that SMARCA4 loss causes dedifferentiation. Herein, using gene editing, we reveal that when serially passaged in mice, SMARCA4-deficient endometrial cancer cells repeatably and predictably generate heterogeneous admixtures of differentiated and undifferentiated cells, resembling human DDEC. Surprisingly, despite this metamorphosis, SMARCA4 loss does not induce lineage plasticity nor reprogramming to a less differentiated fate. Rather, single-cell sequencing combined with barcoding demonstrated that SMARCA4 loss induces a dysregulated epigenome that allows cells to randomly move through cellular states that are otherwise shared with SMARCA4-expressing well-differentiated cancer cells. This finding was validated using a cohort of patient samples, such that epithelial fate markers (E-CADHERIN) can be detected in morphologically undifferentiated cells. Collectively, this work constitutes the first repeatable model of human dedifferentiated cancer and suggests that histological dedifferentiation is not due to the acquisition of a stem cell-like fate. Rather, undifferentiated tissue emerges due to epigenomic dysfunction concomitant with the arbitrary movement of cancer cells between cellular states.

cancer biology↗

Gonadal Hormone Status Dictates Neurobehavioral, Metabolic and Immunological Benefits of Ketogenic Diet in Female Mice through Gut-Metabolic-Brain Axis

The ketogenic diet (KD) is recognized for its broad therapeutic potential across metabolic, neurological, immunological, and aging-related domains; however, its efficacy and durability in females remain underexplored. This study investigated the effects of a short-term, intermittent KD on neurobehavioral function, lipid metabolism, immune response, and gut microbiota composition in sham-operated (intact) and ovariectomized (OVX, estrogen-deficient) female mice, aiming to delineate the interactions between diet and gonadal hormones. In sham females, KD reduced circulating estradiol levels and induced low-grade systemic inflammation, without producing measurable behavioral benefits. Conversely, KD exhibited reduced compulsivity, anxiety, and depression-like behaviors with improved well-being in OVX females, suggesting enhanced neurobehavioral resilience under estrogen-deficient conditions. Biochemical analyses revealed KD-induced hyperlipidemia in both groups, although the lipid load was attenuated in OVX mice. KD further decreased low-density lipoprotein cholesterol but led to uremia and histopathological evidence of hepatic steatosis and fibrosis in OVX females, despite unaltered liver function markers. 16S rRNA sequencing revealed hormone-dependent remodelling of the gut microbiota, characterised by distinct compositional shifts between the sham and OVX cohorts. Correlation analyses linked microbial alterations to improved lipid profiles and reduced anxiodepressive behaviors, implicating the gut-metabolic-brain axis in mediating the effects of KD. Collectively, these findings suggest that KD confers neurobehavioral and metabolic benefits in the absence of ovarian hormones but may also pose risks to the liver and kidneys. These results highlight ketogenic nutrition as a potential non-pharmacological strategy to mitigate menopause- and aging-associated neurobehavioral, metabolic, and immune dysfunctions through modulation of the gut microbiota.

neuroscience↗

Neural manifolds that orchestrate walking and stopping

Walking, stopping and maintaining posture are essential motor behaviors, yet the underlying neural processes remain poorly understood. Here, we investigate neural activity behind locomotion and its walk-to-stop transition. Based on a new theory of the lumbar spinal cord1, 2 we propose and predict that spinal population activity contains limit cycle dynamics to drive walking and fixed-point attractors for stopping. To test these predictions we record neural activity in lumbar cord of freely moving rats using Neuropixels probes3. To control stopping, we stimulate a brainstem nucleus, known to induce motor arrest4-7. We find: During locomotion, the population activity of lumbar spinal neurons exhibits rotational dynamics8-10. These dynamics unfold within a low-dimensional locomotor manifold11, 12, a looping set of trajectories that serves as the repeating signature of locomotion, that also behaves as a limit-cycle attractor. Shortly before stopping, the neural state rapidly changes from the locomotor manifold to a postural fixed point attractor. When kicking the state out of the fixed point using perturbations it shifts to a nearby albeit different fixed point. Repeated stoppings form a local quasi-continuum of fixed points representing various poses - i.e. a postural manifold. These observations are in agreement with our theory, which further indicates the mechanistic roles for subpopulations of spinal interneurons for controlling walking and stopping. Besides explaining the data, our theory makes further predictions to be tested in future experiments.

neuroscience↗

Homocitrullinated Peptides Drive Pro-Inflammatory T-Cell Responses in a Humanized Mouse Model of Rheumatoid Arthritis

ObjectiveAnti-homocitrullinated protein/peptide antibodies (AHCPA) are specific to rheumatoid arthritis (RA) and predictive of worse prognosis, suggesting a pathogenic role for autoreactivity to homocitrullinated antigens. However, T-cell responses to homocitrullinated peptides remain largely unexplored. We investigated these responses in a humanized HLA-DR4-transgenic (DR4tg) mouse model of RA, which expresses the strongest genetic risk factor for this disease. MethodsDR4tg mice were injected subcutaneously with a homocitrullinated peptide called HomoCitJED while control mice received phosphate-buffered saline. After 10 days, T-cells were analyzed for their phenotypic characteristics, cytokine production, and proliferative capacities in the draining lymph nodes (dLNs) and spleens by flow cytometry, enzyme-linked immunosorbent assays, and ProQuantum immunoassays. ResultsHomoCitJED immunization drove robust expansion of T helper (Th) 1, Th17 and hybrid Th1/Th17 CD4+ T cells in dLNs, alongside elevated CD25 activation marker within these subsets. Intracellular cytokine staining confirmed effector activity, revealing higher frequencies of IL-17A+, TNF-+IL-17A+, and IFN-{gamma}+IL-17A+ CD4+ T cells. CD4+ T cells from dLNs also up-regulated the exhaustion markers LAG-3 and Tim-3. CD8+ T cells (Tc) mirrored these findings, as HomoCitJED immunization augmented CD25 and KLRG1 expression, Tc1/Tc17-type IL-17A and IFN-{gamma}/IL-17A production, and antigen-specific proliferation. Additionally, Tim-3, LAG-3 and PD-1 expression on these subsets was augmented. ConclusionsA homocitrullinated peptide elicited Th1/Th17 and Tc1/Tc17 responses marked by concurrent activation and exhaustion signatures, pointing to a dysregulated T-cell state. These findings position homocitrulline-driven T-cell imbalance across both CD4+ and CD8+ T-cell compartments as a potential mechanistic contributor to RA pathogenesis and a target for future immunomodulatory therapies.

immunology↗

Role of zinc in growth, stress response and virulence gene expression of pathogenic Mucorale Rhizopus arrhizus

During COVID-19 pandemic, the cases of mucormycosis increased substantially, with rhino-orbito-cerebral form linked to uncontrolled diabetes being the predominant manifestation. Some clinical and epidemiological studies associated the usage of zinc supplements with the occurrence of COVID-19 associated mucormycosis, but experimental evidence remains limited. This study aimed to elucidate the impact of zinc enrichment on Rhizopus arrhizus, the predominant causative agent of mucormycosis. The effect of zinc supplementation (5 to 150 {micro}M) on fungal growth, metabolic activity, antifungal susceptibility and biofilm formation, along with cell-wall (Congo red), oxidative (hydrogen peroxide) and osmotic (sodium chloride) stress was evaluated in RPMI-1640. Morphological changes were visualized by scanning electron microscopy. Gene expression was monitored by RNA sequencing. Zinc supplementation promoted R. arrhizus growth in a concentration-dependent manner, with the effect being particularly pronounced under less-favorable conditions, such as alkaline conditions resembling the nasal pH of diabetics. Exposure to zinc enhanced the metabolic activity, and partly alleviated the cell-wall and oxidative stress. Susceptibility to amphotericin B and posaconazole was unchanged. Zinc-supplemented cultures over-expressed multiple genes, notably those associated with respiratory electron transport chain, ergosterol biosynthesis, chitosan production, oxidative stress response, mucoricin, high-affinity iron permease, iron transport multi-copper oxidase and ferric-reductase-like protein. Zinc also augmented the growth/metabolism of several other Mucorales but not Aspergillus fumigatus and Candida albicans. The findings suggest that zinc supplementation supports mucoralean growth and enhances the expression of key virulence factors, implying that excessive intake of zinc supplements during COVID-19 pandemic likely contributed to the emergence of mucormycosis. IMPORTANCEMucormycosis remains a highly devastating fungal infection that presented additional challenges during the COVID-19 pandemic. Several risk factors were implicated in the emergence of COVID-19 associated mucormycosis (CAM), including inappropriate corticosteroid usage and COVID-19 associated glycemic imbalance. The excessive intake of nutritional supplements, especially that of zinc, owing to self-medication and over-prescription, was also proposed as a plausible factor in the rise of CAM in many clinical/epidemiological studies. This study experimentally evaluated the potential impact of zinc enrichment on pathogenic Mucorales. The work demonstrates that zinc supplementation supports Rhizopus arrhizus growth, metabolism and stress response, and enhances the expression of key virulence factors, including mucoricin and iron transporters. Notably, the augmentation was specifically observed in pathogenic Mucorales but not Aspergillus fumigatus and Candida albicans. The work provides experimental evidence for the potential association of zinc over-availability with the occurrence of CAM, and strengthens evidence-based therapeutic practices in clinical settings.

microbiology↗

The Influence of Force Field Perturbations on Symmetric and Asymmetric Bimanual Reaching

Bimanual symmetric and asymmetric reaching movements require the motor system to coordinate the two limbs under varying spatial and physical demands. While prior research has shown a strong tendency for temporal synchronization between the hands, little is known about how bimanual reaching is organized when each limb is subjected to distinct types of force fields, such as viscous or elastic loads. This study systematically investigated how matched (viscous/viscous, elastic/elastic) and mismatched (e.g., viscous/no load, elastic/no load, viscous/elastic) load conditions influence key timing and kinematic parameters during bimanual reaching tasks across different spatial configurations and force magnitudes. Results show that kinematic measures for each arm, including peak velocity, peak acceleration, and peak deceleration, exhibit significant differences across both matched and mismatched load conditions, reflecting clear adaptations in limb behavior. In contrast, temporal aspects of movement--specifically the timepoints of peak velocity, peak acceleration, peak deceleration, and movement end time--remain coupled under matched loads but become decoupled under mismatched loads, with each limb operating more independently regardless of the spatial configuration of the task. Together, these findings clarify how the motor system balances the need for coordinated bimanual performance with the flexibility required to adapt to varying load conditions. This study extends prior work by demonstrating that not all bimanual reaches are temporally synchronized; instead, task-specific factors such as load type and symmetry critically shape how the limbs coordinate, revealing the motor systems capacity for flexible, context-dependent control.

neuroscience↗