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Adams, E.

Publications and source records attributed to Adams, E..

18 recordsLinked to original sources

The first OpenBind release: An open experimental structure-affinity dataset and benchmark for structure-based AI

High-quality experimental datasets that link protein-ligand structures with binding affinity data are essential for developing and evaluating structure-based machine learning methods. To help address this need, we established OpenBind as an open-science initiative to generate large-scale experimental datasets for structure-based AI and molecular discovery. Here, we describe the first public OpenBind release, which, to the best of our knowledge, is the largest public single-target experimental structure-affinity dataset. The dataset focuses on enteroviral 2A protease, comprising 925 crystallographic binding events from 699 compounds and associated affinity measurements for 601 compounds. It combines structures from an initial fragment screen and follow-on molecules, together with affinity data, linking experimentally determined protein-ligand binding modes to biophysical measurements within a coherent antiviral discovery campaign. We used this dataset to evaluate protein-ligand structure prediction, binding-affinity prediction, and virtual screening using representative structure-based methods, including docking and cofolding. This exposed several challenges that are central to practical structure-based modelling: docking performance depends strongly on binding-pocket conformation, poses are difficult to rank, and structure-based affinity prediction remains challenging. Fine-tuning OpenFold3-p2 on the fragment-screen structures substantially improved pose prediction and virtual screening for related follow-on compounds, demonstrating how early-stage experimental structures can support target-specific model adaptation.

bioinformatics↗

Targeting AXL Overcomes Adaptive Resistance to KRAS Inhibition in KRAS-Driven Cancer

Direct KRAS inhibitors have established mutant KRAS as a clinically actionable target, yet adaptive resistance remains a major barrier to durable responses. To identify therapeutically actionable resistance mechanisms, we performed an unbiased in vivo CRISPR activation screen in an autochthonous lung adenocarcinoma model, identifying the receptor tyrosine kinase AXL as a dominant adaptive resistance driver. Pharmacologic AXL inhibition enhanced the efficacy of both allele-specific inhibition and the RAS(ON) multi-selective inhibitor daraxonrasib across lung and pancreatic cancer models, resulting in deeper and more durable suppression of MAPK signaling and improved tumor control. Beyond tumor-intrinsic effects, combined KRAS and AXL inhibition remodeled the tumor immune microenvironment, promoting an IFN{gamma}-responsive program, increased recruitment of cytotoxic T cells and sensitization to FAS-mediated apoptosis. Collectively, our findings identify AXL as a convergence point for adaptive resistance to KRAS inhibition and provide a mechanistically informed combination strategy to extend the durability of KRAS-directed therapies. Statement of SignificanceAn unbiased in vivo functional (CRISPR activation) screen identifies AXL as a convergence point for adaptive resistance to KRAS inhibition. By integrating adaptive response to KRAS inhibition with anti-tumor immunity, AXL represents a mechanistically actionable vulnerability whose inhibition deepens and prolongs responses to both allele-specific and pan-KRAS-targeted therapies.

cancer biology↗

Multimodal characterization of variation in neuronal types in the mouse basal ganglia

AbstractThe basal ganglia (BG) are a set of topographically organized, interconnected structures that are pivotal for regulating volitional movement and other aspects of cognitive, motivational, and affective behavior. Recently generated taxonomies of transcriptomically-defined cell types (T-types) have revealed both fine-grained distinctions in gene expression between neurons in these structures as well as continuous transcriptomic variation across similar T-types1-9, which are both related to location within a structure. However, it remains unclear to what extent these and other cellular properties co-vary with each other. Therefore, we performed Patch-seq experiments10,11 on over 900 neurons in mouse brain slices from BG to provide an integrated view of the co-variation between gene expression, location, physiology, and morphology measured from the same neurons. Medium spiny neurons (MSNs) from both the direct and indirect pathways across the dorsal and ventral striatum follow a gene expression gradient that varies in a dorsolateral to ventromedial direction; we find that this gradient also corresponds with systematic differences in action potential kinetics and dendritic arborization. Our analysis also characterizes additional multimodal dimensions of MSN variation, such as those between direct and indirect pathway neurons and between matrix and striosome neurons. Furthermore, through comparison with Patch-seq data from macaque, we demonstrate that the relationship between the transcriptomic/spatial gradient and electrophysiological and morphological properties is conserved across these two species. We also find that properties of striatal interneurons, such as action potential kinetics, vary across the striatum in a manner consistent with the MSN gradient. Outside the striatum, our multimodal Patch-seq dataset from the globus pallidus, subthalamic nucleus, and substantia nigra enabled us to characterize transcriptomically-defined types and link them to prior descriptions of cell types in these structures. Finally, we examined to what extent the MSN transcriptomic/spatial gradient persisted across different stages of the BG circuit by comparing Patch-seq neurons to reconstructed whole-neuron morphologies and the topography of their interareal projections, finding that the gradient is better preserved in GPe and GPi compared to SNr. Our study links transcriptomic variation across T-types in mouse BG to spatial localization and phenotypic differences at the level of individual cells, improving our understanding of cell type architecture in topographically organized circuits of the brain.

neuroscience↗

A field method to optimize dried blood spot sampling for mercury biomonitoring

O_LIHeavy metals are pervasive environmental contaminants that can impair the health of organisms globally. As the largest anthropogenic source of the potent neurotoxin mercury (Hg), gold mining has amplified these threats throughout the tropics. Consequently, there is a mounting need to monitor Hg contamination of the richest biological communities on Earth. Venous whole blood provides a reliable, nonlethal measurement of recent dietary and site-derived contamination, but collecting and cold-storing samples can be impractical in field conditions. C_LIO_LITo overcome these challenges, we developed and evaluated a method to assay Hg exposure in vascular organisms by measuring the volume of dried blood spots (DBS) in the field, which can be stored at ambient temperatures until analysis. We explored the methods precision and accuracy in estimating whole blood Hg concentrations by collecting paired whole blood and DBS aliquots from birds (n = 527 individuals, 140 species) along a trophic gradient (i.e., granivores to piscivores) in Belize and Peru. C_LIO_LIUsing a Bayesian linear mixed-effects model, we found a highly precise and unbiased relationship between DBS and whole blood total Hg concentrations that was centered at perfect unity (R2 = 0.99; {beta} = 1.00 {+/-} 0.03; 95% CrI: 0.95-1.05). Agreement between individual paired aliquots was more variable, in which approximately 12% of DBS containing at least 1 ng THg differed from whole blood by more than {+/-}20%. However, DBS accuracy increased at higher THg concentrations, suggesting that disagreement at low concentrations is an expected consequence of higher measurement error near the analytical limit of detection of our instruments. C_LIO_LICompared to whole-blood collection and analysis workflows, DBS offer substantial logistical advantages by eliminating cold-chain dependence and reducing transport burden, laboratory handling time, and overall operational costs. Consequently, volume-measured DBS provide a practical and highly reliable alternative for monitoring Hg contamination in both humans and wildlife, particularly for ecological and population-level applications in remote and resource-limited environments. C_LI

pharmacology and toxicology↗

Cortical motor activity modulates respiration and reduces apnoea in neonates

Respiration is governed by a widespread network of cortical and subcortical structures. This complex communication between the brain and lungs is altered in pathological conditions. Apnoea - the cessation of respiration - is a common condition in infants, particularly those born prematurely. Apnoea in infants is believed to relate to immaturity of brainstem respiratory centres; involvement of the cortex in respiration in infants has yet to be explored. We investigated if there was any evidence for cortical coupling with respiration in newborn humans and whether it relates to apnoea. Using simultaneous electroencephalography (EEG) and impedance pneumography we investigated interactions between cortical and respiratory activity (known as cortico-respiratory coupling) using phase-amplitude coupling. We show that cortico-respiratory coupling is present in premature and term newborns (104 recordings from 68 infants; 34.5 {+/-} 2.6 weeks post-menstrual age), identifying an interplay between breathing phase and EEG amplitude. We further shed light on the biological meaning by revealing that the strongest coupling occurs during inspiration and that cortical activity precedes respiration, with coupling strongest over frontocentral regions. Whilst our study was limited in spatial resolution, and determining causality is challenging, we believe these findings support the notion that the cortico-respiratory coupling observed here constitutes communication between cortical motor areas and lung effectors. Moreover, we show that cortico-respiratory coupling is negatively correlated with the rate of apnoea, revealing novel insight into this common and potentially life-threatening neonatal pathology.

neuroscience↗

Genome modeling and design across all domains of life with Evo 2

All of life encodes information with DNA. While tools for sequencing, synthesis, and editing of genomic code have transformed biological research, intelligently composing new biological systems would also require a deep understanding of the immense complexity encoded by genomes. We introduce Evo 2, a biological foundation model trained on 9.3 trillion DNA base pairs from a highly curated genomic atlas spanning all domains of life. We train Evo 2 with 7B and 40B parameters to have an unprecedented 1 million token context window with single-nucleotide resolution. Evo 2 learns from DNA sequence alone to accurately predict the functional impacts of genetic variation--from noncoding pathogenic mutations to clinically significant BRCA1 variants--without task-specific finetuning. Applying mechanistic interpretability analyses, we reveal that Evo 2 autonomously learns a breadth of biological features, including exon-intron boundaries, transcription factor binding sites, protein structural elements, and prophage genomic regions. Beyond its predictive capabilities, Evo 2 generates mitochondrial, prokaryotic, and eukaryotic sequences at genome scale with greater naturalness and coherence than previous methods. Guiding Evo 2 via inference-time search enables controllable generation of epigenomic structure, for which we demonstrate the first inference-time scaling results in biology. We make Evo 2 fully open, including model parameters, training code, inference code, and the OpenGenome2 dataset, to accelerate the exploration and design of biological complexity.

genomics↗

From Mechanistic Interpretability to Mechanistic Biology: Training, Evaluating, and Interpreting Sparse Autoencoders on Protein Language Models

Protein language models (pLMs) are powerful predictors of protein structure and function, learning through unsupervised training on millions of protein sequences. pLMs are thought to capture common motifs in protein sequences, but the specifics of pLM features are not well understood. Identifying these features would not only shed light on how pLMs work, but potentially uncover novel protein biology--studying the model to study the biology. Motivated by this, we train sparse autoencoders (SAEs) on the residual stream of a pLM, ESM-2. By characterizing SAE features, we determine that pLMs use a combination of generic features and family-specific features to represent a protein. In addition, we demonstrate how known sequence determinants of properties such as thermostability and subcellular localization can be identified by linear probing of SAE features. For predictive features without known functional associations, we hypothesize their role in unknown mechanisms and provide visualization tools to aid their interpretation. Our study gives a better understanding of the limitations of pLMs, and demonstrates how SAE features can be used to help generate hypotheses for biological mechanisms. We release our code, model weights and feature visualizer.

bioinformatics↗

Sensory event-related potential morphology predicts age in premature infants

Preterm infants undergo substantial neurosensory development in the first weeks after birth. Infants born prematurely are more likely to have long-term adverse neurological outcomes and early detection of abnormal brain development is essential for timely interventions. We investigated whether sensory-evoked cortical potentials could be used to accurately estimate the age of an infant. Such a model could be used to identify infants who deviate from normal neurodevelopment by comparing the brain age to the infants postmenstrual age (PMA). Infants aged between 28- and 40-weeks PMA from a training and test sample (consisting of 101 and 65 recording sessions in 82 and 14 infants, respectively) received trains of approximately 10 visual and 10 tactile stimuli (interstimulus interval approximately 10 seconds). PMA could be predicted accurately from the magnitude of the evoked responses (training set mean absolute error (MAE and 95% confidence intervals): 1.41 [1.14; 1.74] weeks, p = 0.0001; test set MAE: 1.55 [1.21; 1.95] weeks, p = 0.0002. Moreover, we show with two examples that brain age, and the deviations between brain age and PMA, may be biologically and clinically meaningful. By firstly demonstrating that brain age is correlated with a measure known to relate to maturity of the nervous system (based on animal and human literature, the magnitude of reflex withdrawal is used) and secondly by linking brain age to long-term neurological outcomes, we show that brain age deviations are related to biologically meaningful individual differences in the rate of functional nervous system maturation rather than noise generated by the model. In summary, we demonstrate that sensory-evoked potentials are predictive of age in premature infants. It takes less than 5 minutes to collect the stimulus electroencephalographic data required for our model, hence, increasing its potential utility in the busy neonatal care unit. This model could be used to detect abnormal development of infants response to sensory stimuli in their environment and may be predictive of later life abnormal neurodevelopmental outcome.

neuroscience↗

Examining the effectiveness of blanket curtailment strategies in reducing bat fatalities at terrestrial wind farms in North America

Blanket curtailment of turbine operations during low wind conditions has become an accepted operational minimization tactic to reduce bat mortality at terrestrial wind facilities. Site-specific studies have demonstrated that operational curtailment effectively reduces impacts, but the exact nature of the relationship between increased cut-in speed and fatality reduction in bats remains unclear. To evaluate the efficacy of differing blanket curtailment regimes in reducing bat fatality, we examined data from turbine curtailment experiments in the United States and Canada in a meta-analysis framework. We tested multiple statistical models to explore possible linear and non-linear relationships between turbine cut-in speed and bat fatality reduction while controlling for control cut-in speed. Because the overall sample size for this meta-analysis was small (n = 36 control-treatment studies from 16 field sites from the American Wind Wildlife Information Center and a recent review), we conducted a power analysis to assess the number of control-impact curtailment studies that would be needed to understand the relationship between fatality rate and change in cut-in speed under different fatality reduction scenarios. We also identified the characteristics of individual field studies that may influence their power to detect fatality reduction due to curtailment. Using a response ratio approach, we found any curtailment strategy reduced fatality rates by 56% for studies included in this analysis (p < 0.001). However, we did not find strong evidence for linear (p =0 0.07) or non-linear (p > 0.11) associations between increasing cut-in speeds and fatality reduction. The power analyses showed that the power to detect effects in the meta-analysis was low if fatality reductions were less than 50%. Synthesizing across all analyses, we need more well-designed curtailment studies to determine the effect of increasing curtailment speed and the effect size is likely of a magnitude that we had limited power to detect.

ecology↗

The Forget-Me-Not dHCP study: 7 Tesla high resolution diffusion imaging in the unfixed post-mortem neonatal brain

Diffusion MRI of the neonatal brain allows investigation of the organisational structure of maturing fibres during brain development. Post-mortem imaging has the potential to achieve high resolution by using long scan times, enabling precise assessment of small structures. The Forget-Me-Not study, part of the Developing Human Connectome Project (dHCP), aims to acquire and publicly distribute high-resolution diffusion MRI data for unfixed post-mortem neonatal brain at 7T with a custom-built head coil. This paper describes how the study addressed logistical, technical and ethical challenges relating to recruitment pipeline, care pathway, tissue preservation, scan setup and protocol optimisation. Results from the first subject recruited to the study demonstrate high-quality diffusion MRI data. Preliminary voxel-wise and tractography-based analyses are presented for the cortical plate, subplate and white matter pathways, with comparison to age-matched in vivo dHCP data. These results demonstrate that high quality post-mortem data can be acquired and provide a sensitive means to explore the developing human brain, as well as altered diffusion properties consistent with post-mortem changes, at high resolution.

bioengineering↗

A highly multiplexed melt-curve assay for detecting the most prevalent carbapenemase, ESBL and AmpC genes

Resistance to third generation cephalosporins and carbapenems in Gram-negative bacteria is chiefly mediated by beta-lactamases including ESBL, AmpC and carbapenemase enzymes. Routine phenotypic detection methods do not provide timely results, and there is a lack of comprehensive molecular panels covering all important markers. An ESBL/carbapenemase HRM assay (SHV, TEM, CTX-M ESBLs, and NDM, IMP, KPC, VIM and OXA-48-like carbapenemases) and an AmpC HRM assay (16S rDNA control, FOX, MOX, ACC, EBC, CIT and DHA) were designed, and evaluated on 111 Gram-negative isolates with mixed resistance patterns. The sensitivity for carbapenemase, ESBL and AmpC genes was 96.7% (95%CI:82.8-99.9%), 93.6% (95%CI:85.7-97.9%) and 93.8% (95%CI:82.8-98.7%), respectively with a specificity of 100% (95%CI:95.6-100%), 93.9% (95%CI:79.8-99.3%) and 93.7% (95%CI:84.5-98.2%). The HRM assays enable the simultaneous detection of the fourteen most important ESBL, carbapenemase and AmpC genes and could be used as a molecular surveillance tool or to hasten detection of AMR for treatment management.

microbiology↗

Laboratory Analysis of an Outbreak of Candida auris in New York from 2016 to 2018-Impact and Lessons Learned

Candida auris is a multidrug-resistant yeast which has emerged in healthcare facilities worldwide, however little is known about identification methods, patient colonization, spread, environmental survival, and drug resistance. Colonization on both biotic and abiotic surfaces, along with travel, appear to be the major factors for the spread of this pathogen across the globe. In this investigation, we present laboratory findings from an ongoing C. auris outbreak in NY from August 2016 through 2018. A total of 540 clinical isolates, 11,035 patient surveillance specimens, and 3,672 environmental surveillance samples were analyzed. Laboratory methods included matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) for yeast isolate identification, real-time PCR for rapid surveillance sample screening, culture on selective/non-selective media for recovery of C. auris and other yeasts from surveillance samples, antifungal susceptibility testing to determine the C. auris resistance profile, and Sanger sequencing of ribosomal genes for C. auris genotyping. Results included: a) identification and confirmation of C. auris in 413 clinical isolates and 931 patient surveillance isolates, as well as identification of 277 clinical cases and 350 colonized cases from 151 healthcare facilities including 59 hospitals, 92 nursing homes, 1 long-term acute care hospital (LTACH), and 2 hospices, b) successful utilization of an in-house developed C. auris real-time PCR assay for the rapid screening of patient and environmental surveillance samples, c) demonstration of relatively heavier colonization of C. auris in nares compared to the axilla/groin, and d) predominance of the South Asia Clade I with intrinsic resistance to fluconazole and elevated minimum inhibitory concentration (MIC) to voriconazole (81%), amphotericin B (61%), 5-FC (3%) and echinocandins (1%). These findings reflect greater regional prevalence and incidence of C. auris and the deployment of better detection tools in an unprecedented outbreak.

microbiology↗

Machine learning predicts rapid relapse of triple negative breast cancer

PurposeMetastatic relapse of triple-negative breast cancer (TNBC) within 2 years of diagnosis is associated with particularly aggressive disease and a distinct clinical course relative to TNBCs that relapse beyond 2 years. We hypothesized that rapid relapse TNBCs (rrTNBC; metastatic relapse or death <2 years) reflect unique genomic features relative to late relapse (lrTNBC; >2 years).\n\nPatients and MethodsWe identified 453 primary TNBCs from three publicly-available datasets and characterized each as rrTNBc, lrTNBC, or no relapse (nrTNBC: no relapse/death with at least 5 years follow-up). We compiled primary tumor clinical and multi-omic data, including transcriptome (n=453), copy number alterations (CNAs; n=317), and mutations in 171 cancer-related genes (n=317), then calculated published gene expression and immune signatures.\n\nResultsPatients with rrTNBC were higher stage at diagnosis (Chi-square p<0.0001) while lrTNBC were more likely to be non-basal PAM50 subtype (Chi-square p=0.03). Among 125 expression signatures, five immune signatures were significantly higher in nrTNBCs while lrTNBC were enriched for eight estrogen/luminal signatures (all FDR p<0.05). There was no significant difference in tumor mutation burden or percent genome altered across the groups. Among mutations, only TP53 mutations were significantly more frequent in rrTNBC compared to lrTNBC (Fisher exact FDR p=0.009). To develop an optimal classifier, we used 77 significant clinical and omic features to evaluate six modeling approaches encompassing simple, machine learning, and artificial neural network (ANN). Support vector machine outperformed other models with average receiver-operator characteristic area under curve >0.75.\n\nConclusionsWe provide a new approach to define TNBCs based on timing of relapse. We identify distinct clinical and genomic features that can be incorporated into machine learning models to predict rapid relapse of TNBC.

cancer biology↗

Spatio-Temporal Dynamics of Landscape Use by the Bumblebee Bombus atratus (Hymenoptera: Apidae) and its relationship with pollen provisioning.

Understanding how bees use resources at a landscape scale is essential for developing meaningful management plans that sustain populations and the pollination services they provide. Bumblebees are important pollinators for many wild and cultivated plants, and have experienced steep population declines worldwide. Bee foraging behavior can be influenced by resource availability and the bees lifecycle stage. To better understand these relationships, we studied the habitat selection of Bombus atratus by tracking 17 queen bumblebees with radio telemetry in blueberry fields in Entre Rios province, Argentina. To evaluate land use and floral resources used by bumblebees, we tracked bees before and after nest establishment and estimated home ranges using minimum convex polygons and kernel density methods. We also classify the pollen of their body to determine which botanical resources they use from the floral species available. We characterized land use for each bee as the relative proportion of GPS points inside of each land use. Bumblebees differed markedly in their movement behavior in relation to nest establishment. They moved over larger areas and mostly within blueberry fields before to nest establishment, in contrast to after establishing the nest that they preferred the edges near forest plantations and changed the nutritional resources by wild floral species. Our study is the first to track queen bumblebee movements in an agricultural setting and relate movement change across time and space with pollen resource availability. This study provides insight into the way bumblebee queens use different habitat elements at crucial periods in their lifecycle, showing the importance of mass flowering crops like blueberry in the first stages of queens lifecycle and how diversified landscapes help support bee populations as their needs changes during different phases of their lifecycle.

ecology↗

Loss of tau and Fyn reduces compensatory effects of MAP2 for tau and reveals a Fyn-independent effect of tau on glutamate-induced Ca2+ response

Microtubule-associated protein tau associates with Src family tyrosine kinase Fyn. A tau-Fyn double knockout (DKO) mouse was generated to investigate the role of the complex. DKO mice resembled Fyn KO in cognitive tasks and resembled tau KO mice in motor tasks and protection from pentylenetetrazole-induced seizures. In Ca2+ response, Fyn KO was decreased relative to WT and DKO had a greater reduction relative to Fyn KO, suggesting that tau may have a Fyn-independent role. Since tau KO resembled WT in its Ca2+ response, we investigated whether MAP2 served to compensate for tau, since its level was increased in tau KO but decreased in DKO mice. We found that like tau, MAP2 increased Fyn activity. Moreover, tau KO neurons had increased density of dendritic MAP2-Fyn complexes relative to WT neurons. Therefore, we hypothesize that in the tau KO, the absence of tau would be compensated by MAP2, especially in the dendrites, where tau-Fyn complexes are of critical importance. In the DKO, decreased levels of MAP2 made compensation more difficult, thus revealing the effect of tau in the Ca2+ response.\n\nSummary StatementThe downstream effect of the interaction between microtubule-associated protein tau and Src family non-receptor tyrosine kinase Fyn was investigated with a tau/Fyn double KO mouse. We demonstrate that tau has a Fyn-independent role in glutamate-induced calcium response and that MAP2 can compensate for tau in interacting with Fyn in dendrites.

neuroscience↗

TCR-pMHC bond length controls TCR ligand discrimination

T-cell receptors (TCRs) detect specifically and sensitively a small number of agonist peptide-major histocompatibility complexes (pMHCs) from an ocean of structurally similar self-pMHCs to trigger antigen-specific adaptive immune responses1-4. Despite intense efforts, the mechanism underlying TCR ligand discrimination remains a major unanswered question in immunology. Here we show that a TCR discriminates between closely related peptides by forming TCR-pMHC bonds with different lengths, which precisely control the accessibility of CD3{zeta} immunoreceptor tyrosine-based activation motifs (ITAMs) for phosphorylation. Using in situ fluorescence resonance energy transfer (FRET)3,5, we measured the intermolecular length of single TCR-pMHC bonds and the intramolecular distance of individual TCR-CD3{zeta} complexes at the membrane of live primary T cells. We found that an agonist forms a short TCR-pMHC bond to pull the otherwise sequestered CD3{zeta} off the inner leaflet of the plasma membrane, leading to full exposure of its ITAMs for strong phosphorylation. By contrast, a structurally similar weaker peptide forms a longer bond with the TCR, resulting in partial dissociation of CD3{zeta} from the membrane and weak phosphorylation. Furthermore, we found that TCR-pMHC bond length determines 2D TCR binding kinetics and affinity, T-cell calcium signaling and T-cell proliferation, governing the entire process of signal reception, transduction and regulation. Thus, our data reveal the fundamental mechanism by which a TCR deciphers the structural differences between foreign antigens and self-peptides via TCR-pMHC bond length to initiate different TCR signaling for ligand discrimination.

immunology↗

Characterization of osteoarthritis phenotypes by global metabolomic profiling of human synovial fluid

ObjectiveOsteoarthritis (OA) is a multifactorial disease with etiological heterogeneity. The objective of this study was to classify OA subgroups by generating metabolic phenotypes of OA from human synovial fluid.\n\nDesignPost mortem synovial fluids (n=75) were analyzed by high performance-liquid chromatography mass spectrometry (HPLC-MS) to measure changes in the global metabolome. Comparisons of healthy (grade 0), early OA (grades I-II), and late OA (grades III-IV) donor populations were considered to reveal phenotypes throughout disease progression.\n\nResultsGlobal metabolomic profiles in synovial fluid were distinct between healthy, early OA, and late OA donors. Pathways differentially activated among these groups included structural deterioration, glycerophospholipid metabolism, inflammation, central energy metabolism, oxidative stress, and vitamin metabolism. Within disease states (early and late OA), subgroups of donors revealed distinct phenotypes. Phenotypes of OA exhibited increased inflammation (early and late OA), oxidative stress (late OA), or structural deterioration (early and late OA) in the synovial fluid.\n\nConclusionThese results revealed distinct metabolic phenotypes of OA in human synovial fluid, provide insight into pathogenesis, represent novel biomarkers and assist in developing personalized interventions for subgroups of OA patients.

pathology↗

CD4+ T cell fate decisions are stochastic, precede cell division, depend on GITR co-stimulation, and are associated with uropodium development

During an immune response, naive CD4+ T cells proliferate and generate a range of effector, memory and regulatory T cell subsets, but how these processes are co-ordinated remains unclear. A traditional model suggests that memory cells use mitochondrial respiration and are survivors from a pool of previously proliferating and glycolytic, but short-lived effector cells. A more recent model proposes a binary commitment to either a memory or effector cell lineage during a first, asymmetric cell division, with each lineage able to undergo subsequent proliferation and differentiation. We used improved fixation and staining methods with imaging flow cytometry in an optimised in vitro system that indicates a third model. We found that cell fates result from stochastic decisions that depend on GITR co-stimulation and which take place before any cell division. Effector cell commitment is associated with mTORC2 signalling leading to uropodium development, while developing memory cells lose mitochondria, have a nuclear localization of NF{kappa}B and depend on TGF{beta} for their survival. Induced, T helper subsets and foxp3+ regulatory T cells were found in both the effector and memory cell lineages. This in vitro model of T cell differentiation is well suited to testing how manipulation of cytokine, nutrient other components of the microenvironment might be exploited for therapeutic purposes.

immunology↗