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Martinez, R.

Publications and source records attributed to Martinez, R..

At least 19 recordsLinked to original sources

A platform for automated training of mammalian cell physiology

Controlling cell physiology is difficult, not only because of cells complexity, but also their capacity for real-time adaptation to interventions, leading to challenges such as drug resistance and transgene silencing. Accumulating evidence suggests that this adaptivity resembles classical forms of learning defined in behavioral science. However, a lack of appropriate platforms has led to gaps in our understanding of cells capacity for adaptive problem-solving in physiological and transcriptional space. Here, we present a device, the Cell Trainer, capable of performing a wide variety of automated training experiments on non-neural mammalian cells, using timed drug pulses as the stimulus, and a mobile fluorescence microscope to capture images of responses, across replicate cultures. The Cell Trainer can operate in either an open-loop (feedforward) or closed-loop (feedback-controlled) mode, and our image analysis pipeline can report the behaviors of individual cells throughout each experiment and quantify population heterogeneity. We showcase the ability of the Cell Trainer to execute experimental protocols and perform single-cell analyses in both modes. We first demonstrate with a feedforward experiment in which myoblasts are repeatedly pulsed with dimethyl sulfoxide (DMSO) and their discrete calcium responses are analyzed, revealing sensitization-like dynamics. Next, we demonstrate a feedback control scheme wherein the fluorescence of a pH/voltage reporter in kidney cells is maintained below a threshold level with controlled pulses of acid. To accelerate research in the field of cell training, learning, and memory, we are openly sharing the Cell Trainer schematics and software with the research community. This platform provides a flexible tool for studying how cellular physiological states can be shaped by patterned stimulation and feedback control through approaches that work with the native adaptive competencies of cells.

bioengineering↗

Microbial, dietary insect, and pathogen communities in fresh and decomposing guano of anthropic little brown bat (Myotis lucifugus) maternity colonies

The guano of insectivorous bats holds ecological information that can be assessed non-invasively to characterize the gut microbiome and diet, alongside environmental microbes and pathogens of conservation concern. Despite this potential, how guano communities change during decomposition remains understudied, particularly inside anthropic roosts rather than caves. In this study, guano from little brown bat (Myotis lucifugus) colonies was sampled monthly across the summer maternity season from three sites across two locations in Connecticut, USA, at fresh deposition and at 4, 8, and 12 weeks following deposition. Resolving these cross-kingdom signals required five workflows: short-read 16S and ITS2 amplicon sequencing (Illumina) for bacterial and fungal profiling, long-read CO1 metabarcoding (Oxford Nanopore) for arthropod diet in fresh samples, long-read shotgun metagenomics for viral identification in aged samples, and targeted qPCR for organisms of bat, human, and forest-health concern. Fresh guano generated a consistent bacterial signal across sites, whereas fresh fungal communities differed by site. Responses to decomposition depended on roost setting: exterior sites lost fungal diversity and shifted toward environmental aerobes over time, while the interior roost retained the fresh sample profile. Dietary composition varied temporally, was dominated by Diptera, and included the invasive emerald ash borer (Agrilus planipennis). Pseudogymnoascus destructans, the causal agent of white-nose syndrome, occurred in fresh and aged samples at all three sites but persisted for 12 weeks only at the interior roost, where antifungal bacterial taxa were depleted. Long-read shotgun metagenomics of aged guano recovered roughly 100 viral species, predominantly bacteriophages, alongside non-bacteriophage mastadenoviruses associated with humans, bats, and other mammals. These results show that anthropic structures influence the trajectory of guano microbiome succession, and that maternity colony guano enables non-invasive assessment of environmental pathogens, bat diet, and bacterial and fungal communities.

ecology↗

Enhancer-based AAV approach for selective AADC delivery reduces motor symptoms and dyskinesia in Parkinson's mouse models

Degeneration of midbrain dopamine (DA) neurons and the resulting loss of striatal dopamine signaling are hallmarks of Parkinsons disease (PD). Although the dopamine precursor levodopa (L-DOPA) provides symptomatic relief, prolonged treatment often leads to abnormal involuntary movements (dyskinesia). Previous adeno-associated virus (AAV) approaches delivering aromatic L-amino acid decarboxylase (AADC) to the striatum under a ubiquitous promoter enhanced local dopamine synthesis and improved PD motor deficits, but this broad targeting strategy limited insight into the cellular populations underlying the behavioral improvements. Here, we engineered enhancer-driven AAVs to direct AADC expression to defined striatal and midbrain cell populations and paired these regulatory elements with a blood-brain barrier-penetrant capsid to enable both systemic and direct delivery. Targeted expression restored motor performance at reduced L-DOPA doses and decreased dyskinesia-like behaviors, producing improvements comparable to or greater than those achieved with ubiquitous expression. Distinct neuronal and non-neuronal populations each supported motor rescue but improved different behavioral domains to different extents, indicating complementary cell type-specific roles within PD-relevant circuits. Together, these findings establish enhancer-driven, cell type-specific AADC delivery as a better-tolerated strategy that enables rescue of motor deficits at lower L-DOPA doses in PD models.

neuroscience↗

Particle-based hydrogel inks and support matrices for biofabricating structural complexity, soluble gradients, and cell-lined channels in fully granular bioprinted systems

Towards achieving biomimetic complexity in biofabricated systems, an all-granular bioprinting system might use particle-based hydrogel inks to establish structures within a particle-based support matrix. In such a system, the granular support matrix can be designed to persist in the final construct and include cells incorporated prior to printing. To biofabricate complexity, bioprinting can introduce high-resolution heterogeneous structures that guide cell behaviors. The designs of the granular ink and support hydrogels are crucial to achieving complexity. High resolution structures and channels depend on small particles that flow and can be stabilized, and that can be printed and then removed, respectively. Herein, an all-granular system is described that used a granular formulation of an established, tunable hyaluronic acid-based hydrogel as the basis for a support matrix and a small particle gelatin hydrogel as an ink. Towards facilitating stabilization of the printed structure and flow during printing, the support and ink materials included soluble, interstitial components, and all exhibited yield stress behaviors characteristic of granular hydrogel systems. The support matrixs viscoelastic properties were dependent on intraparticle hydrogel network design, and it could be stabilized against flow by photoinitiated crosslinking. The gelatin ink could form fine filaments, as small as 100 {micro}m in testing here, and melted to leave channels within crosslinked support matrices. Channels could support flows introduced by hydrostatic pressure and could be used to rapidly transport soluble factors into the construct, which could be used to establish soluble gradients by diffusion and support cell viability. The all-granular system supported printing of complex, multimaterial structures, with feature resolution on the order of 100 {micro}m and spatial positioning on the order of 10s {micro}m. The process and materials exhibited biocompatibility with respect to cells included within the support matrix during printing or introduced into channels to begin establishing endothelialized bioprinted vessels.

bioengineering↗

Stress attenuation by the adrenergic-specific lncRNA NESPR prevents cell death in neuroblastoma cells

Neuroblastoma is a pediatric cancer of the sympathetic nervous system characterized by heterogeneous cell states that mirror normal differentiation trajectories. Each state is governed by a core regulatory transcriptional circuitry that reinforces cell identity through an autoregulatory feedforward loop. We identified the long non-coding RNA NESPR as specifically expressed in adrenergic neuroblastoma cells. NESPR expression correlates with high-risk neuroblastoma clinical parameters and poor patient survival. NESPR is located within an insulated gene neighborhood alongside PHOX2B, a master transcription factor of the adrenergic identity. NESPR depletion reduced cell proliferation and increased caspase activity in neuroblastoma cell lines, and NESPR knockout in a neuroblastoma zebrafish model led to reduced tumor penetrance. Subcellular localization revealed NESPR to be a cytosolic long non-coding RNA, suggesting a trans-regulatory function. RNA-sequencing following NESPR depletion revealed a shift from an adrenergic to a mesenchymal cell state, due to proteotoxic stress-induced molecular reprogramming. These findings suggest NESPR as a regulator of neuroblastoma cell identity with potential therapeutic opportunities in high-risk neuroblastoma cases.

genetics↗

Commensal-derived short-chain fatty acids disrupt lipid membrane homeostasis in Staphylococcus aureus

The role of commensal anaerobic bacteria in chronic respiratory infections is unclear, yet they can exist in abundances comparable to canonical pathogens in vivo. Their contributions to the metabolic landscape of the host environment may influence pathogen behavior by competing for nutrients and creating inhospitable conditions via toxic metabolites. Here, we reveal a mechanism by which the anaerobe-derived short chain fatty acids (SCFAs) propionate and butyrate negatively affect Staphylococcus aureus physiology by disrupting branched chain fatty acid (BCFA) metabolism. In turn, BCFA impairment results in impaired growth, diminished expression of the agr quorum sensing system, as well as increased sensitivity to membrane-targeting antimicrobials. Altered BCFA metabolism also reduces S. aureus fitness in competition with Pseudomonas aeruginosa, suggesting that airway microbiome composition and the metabolites they produce and exchange directly impact pathogen succession over time. The pleiotropic effects of these SCFAs on S. aureus fitness and their ubiquity as metabolites in animals also suggests that they may be effective as sensitizers to traditional antimicrobial agents when used in combination.

microbiology↗

Enhancer AAVs for targeting spinal motor neurons and descending motor pathways in rodents and macaque

Experimental access to cell types within the mammalian spinal cord is severely limited by the availability of genetic tools. To enable access to lower motor neurons (LMNs) and LMN subtypes, we generated single cell multiome datasets from mouse and macaque spinal cords and discovered putative enhancers for each neuronal population. We cloned these enhancers into adeno-associated viral vectors (AAVs) driving a reporter fluorophore and functionally screened them in mouse. We extensively characterized the most promising candidate enhancers in rat and macaque and developed an optimized pan LMN enhancer virus. Additionally, we generated derivative viruses expressing iCre297T recombinase or ChR2-EYFP for labeling and functional studies, and we created a single vector with combined enhancer elements to achieve simultaneous labeling of layer 5 extratelencephalic projecting (ET) neurons and LMNs. This unprecedented LMN toolkit will enable future investigations of cell type function across species and potential therapeutic interventions for human neurodegenerative diseases.

neuroscience↗

Recovery mode: Marine protected areas enhance the resilience of kelp species from marine heatwaves

Marine protected areas (MPAs) can promote population recovery from climate change impacts by reducing local stressors, such as fishing. However, with extreme climatic events such as marine heatwaves (MHWs) increasing in frequency and duration, it remains unclear whether MPAs enhance recovery following these acute perturbations, and how recovery varies across species and ecological traits (e.g., sedentary vs mobile species). We used 16 years (2007-2022) of kelp forest monitoring data in Isla Natividad, Baja California Sur, Mexico, to assess the impact of the 2014-2016 MHWs on fish and invertebrate communities. Then we evaluated the impact and recovery from the MHWs of economically and ecologically important invertebrate species inside and outside two fully protected marine reserves. We found that the 2014-2016 MHWs, which were the most intense and persistent ever observed in Isla Natividad, impacted invertebrates but not fish biomass. Marine reserves did not confer resistance to the MHWs, however, reserves did enhance the recovery of some species after the MHWs. Inside marine reserves, abalone (Haliotis spp.) and wavy turban snail (Megastraea spp.) (benthic sedentary invertebrates) recovered to pre-heatwave biomass after two years and spiny lobster (Panulirus interruptus) (benthic mobile invertebrate) after four years. Outside the reserves, abalone recovered after three years, while the other two species never recovered. The warty sea cucumber (Apostichopus parvimensis) population collapsed after the MHWs and never recovered inside nor outside the reserve. Remarkably, abalone biomass had an outstanding and sustained recovery inside reserves, with a 5.6-fold increase in biomass after the MHWs, which was over three times higher than the recovery reported outside the reserve. Our analysis of long-term monitoring data shows that marine reserves cannot prevent adverse impacts from extreme climatic events but can enhance species recovery following these events. Benefits conferred by marine reserves, however, are species-specific and may be limited to species with limited dispersal and localized population dynamics.

ecology↗

Extracellular vesicles produced during fungal infection in humans are immunologically active

Of the known 1.5 million fungal species, Candida spp., Cryptococcus spp., and Paracoccidioides spp. are the main pathogenic species causing serious diseases with almost two million annual deaths. The diagnosis and treatment of fungal infections are challenging since of the limited access to diagnostic tests and the emergence of antifungal resistance. Extracellular vesicles (EVs) promote the interactions of fungal cells with other organisms and play an important role in the pathogen-host relationship. Owing to the complexity of fungal EVs and the lack of clinical studies on their roles in human infections, we studied the EVs from the serum and urine samples of patients with fungal infections caused by Candida albicans, Cryptococcus neoformans, and Paracoccidioides brasiliensis and determined their roles. Steroids, sphingolipids, and fatty acids were identified as the main secondary metabolites via mass spectrometry analysis. We asked whether these metabolites in EVs could play roles in modulating the host immune response. Our findings revealed the polarization of the proinflammatory profile in murine and human macrophages, with the increased production of cytokines, such as the tumor necrosis factor-, interferon-{gamma}, and interleukin-6, and an increased expression of the inducible nitric oxide synthase gene, a M1 response marker. Therefore, circulating EVs from patients with fungal infections are likely involved in the disease pathophysiology. Our findings provide insights into the roles of EVs in fungal infections in clinical samples and in vitro, suggesting possible targets for systemic mycoses therapy. Significance StatementFungal infections cause approximately 1.6 million deaths annually. Due to therapeutic and diagnostic limitations, it is mandatory to understand and develop new immunological interventions. Despite several in vitro studies on the production of extracellular vesicles (EVs) from fungal pathogens, this study is a pioneer in the identification and characterization of EVs in the course of fungal infection in humans. Our group demonstrated the presence of EVs in clinical samples from patients diagnosed with candidiasis, cryptococcosis, and paracoccidioidomycosis, as well as the EVs interaction produced by host and fungal pathogen with the immune system, resulting in relationships that may be beneficial for the progression or elimination of fungal disease.

microbiology↗

Patient phenotypes and their relation to TNFα signaling and immune cell composition in critical illness and autoimmune disease

RationaleTNF inhibitors have shown promise in reducing mortality in hospitalized COVID-19 patients; one hypothesis explaining the limited clinical efficacy is patient heterogeneity in the TNF pathway. MethodsWe evaluated the effect of TNF inhibitors in a mouse model of LPS-induced acute lung injury. Using machine learning we attempted predictive enrichment of TNF signaling in patients with either ARDS or sepsis. We examined biological factors that drive heterogeneity in host responses to critical infection and their relation to clinical outcomes. ResultsIn mice, LPS induced TNF-dependent neutrophilia, alveolar permeability and endothelial injury. In humans, TNF pathway activation was significantly increased in peripheral blood of patients with critical illnesses and associated with the presence of mature neutrophils across critical illnesses and several autoimmune conditions. Machine learning using a gene signature separated patients into 5 phenotypes; one was a hyper-inflammatory, interferon-associated phenotype enriched for increased TNF pathway activation and conserved across critical illnesses and autoimmune diseases. Cell subset profiles segregated severely ill patients into neutrophil-subset-dependent groups that were enriched for disease severity, demonstrating the importance of neutrophils in the immune response in critical illness. ConclusionsTNF signaling and mature neutrophils are associated with a hyper-inflammatory phenotype of patients, shared across critical illness and autoimmune disease. This phenotyping provides a personalized medicine hypothesis to test anti-TNF therapy in severe respiratory illness. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=103 SRC="FIGDIR/small/564631v1_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@1e25724org.highwire.dtl.DTLVardef@c708bcorg.highwire.dtl.DTLVardef@10e7531org.highwire.dtl.DTLVardef@3014b8_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

Acute ampakines increase voiding function and coordination in a rat model of SCI

Neurogenic bladder dysfunction causes urological complications and reduces the quality of life in persons with spinal cord injury (SCI). Glutamatergic signaling via AMPA receptors is fundamentally important to the neural circuits controlling bladder voiding. Ampakines are positive allosteric modulators of AMPA receptors that can enhance the function of glutamatergic neural circuits after SCI. We hypothesized that ampakines can acutely stimulate bladder voiding that has been impaired due to thoracic contusion SCI. Adult female Sprague Dawley rats received a unilateral contusion of the T9 spinal cord (n=10). Bladder function (cystometry) and coordination with the external urethral sphincter (EUS) were assessed five days post-SCI under urethane anesthesia. Data were compared to responses in spinal intact rats (n=8). The "low impact" ampakine CX1739 (5, 10, or 15 mg/kg) or vehicle (HPCD) was administered intravenously. The HPCD vehicle had no discernable impact on voiding. In contrast, following CX1739, the pressure threshold for inducing bladder contraction, voided volume, and the interval between bladder contractions were significantly reduced. These responses occurred in a dose-dependent manner. We conclude that modulating AMPA receptor function using ampakines can rapidly improve bladder voiding capability at sub-acute time points following contusion SCI. These results may provide a new and translatable method for therapeutic targeting of bladder dysfunction acutely after SCI.

neuroscience↗

Stricturing Crohn's disease single-cell RNA sequencing reveals fibroblast heterogeneity and intercellular interactions

BackgroundFibroblasts play a key role in stricture formation in Crohns disease (CD) but understanding its pathogenesis requires a systems-level investigation to uncover new treatment targets. We studied full thickness CD tissues to characterize fibroblast heterogeneity and function by generating the first single cell RNA sequencing (scRNAseq) atlas of strictured bowel and providing proof of principle for therapeutic target validation. MethodsWe performed scRNAseq of 13 fresh full thickness CD resections containing non-involved, inflamed non-strictured, and strictured segments as well as 7 normal non-CD bowel segments. Each segment was separated into mucosa/submucosa or muscularis propria and analyzed separately for a total of 99 tissue samples and 409,001 cells. We validated cadherin-11 (CDH11) as a potential therapeutic target by using whole tissues, isolated intestinal cells, NanoString nCounter, next generation sequencing, proteomics and animal models. ResultsOur integrated dataset revealed fibroblast heterogeneity in strictured CD with the majority of stricture-selective changes detected in the mucosa/submucosa, but not the muscle layer. Cell-cell interaction modeling revealed CXCL14+ as well as MMP/WNT5A+ fibroblasts displaying a central signaling role in CD strictures. CDH11, a fibroblast cell-cell adhesion molecule, was broadly expressed and upregulated, and its pro-fibrotic function was validated by NanoString nCounter, RNA sequencing, tissue target expression, in vitro gain- and loss-of-function experiments, proteomics, and two animal models of experimental colitis. ConclusionA full-thickness bowel scRNAseq atlas revealed previously unrecognized fibroblast heterogeneity and interactions in CD strictures and CDH11 was validated as a potential therapeutic target. These results provide a new resource for a better understanding of CD stricture formation and opens potential therapeutic developments.

immunology↗

Identification of a pharmaceutical biostasis inducer that slows metabolism in multiple vertebrates that do not hibernate

Drugs that induce reversible slowing of metabolic and physiological processes would have great value for organ preservation, especially for organs with high susceptibility to hypoxia-reperfusion injury, such as the heart. Using whole-organism screening of metabolism, mobility, and development in Xenopus, we identified an existing drug, SNC80, that rapidly and reversibly slows biochemical and metabolic activities while preserving cell and tissue viability. Although SNC80 was developed as a delta opioid receptor activator, we discovered that its ability to slow metabolism is independent of its opioid modulating activity as a novel SNC80 analog (WB3) with almost 1,000 times less delta opioid receptor binding activity is equally active. Metabolic suppression was also achieved using SNC80 in microfluidic human organs-on-chips, as well as in explanted whole porcine hearts and limbs, demonstrating the cross-species relevance of this approach and potential clinical relevance for surgical transplantation. Pharmacological induction of physiological slowing in combination with organ perfusion transport systems may offer a new therapeutic approach for tissue and organ preservation for transplantation, trauma management, and enhancing patient survival in remote and low-resource locations.

bioengineering↗

Differential expression analysis of sexual and apomictic Boechera uncovers FAS4 as crucial for gametogenesis

During sexual reproduction of higher plants, seed formation is initiated by double fertilization of egg and central cell. In contrast, pseudogamous apomicts form embryos asexually by parthenogenesis of the egg, but initiation of endosperm development still depends on central cell fertilization. It can be envisioned that these differences are determined during gametogenesis and specification of gametophytic cells. To deepen the understanding of the transcriptional basis underlying sexual and apomictic reproduction, we applied tissue type-specific RNA-Seq. We compared expression in reproductive tissues of different Boechera accessions at distinct developmental stages. This confirmed previous evidence for an enrichment of RNA helicases at onset of reproductive development. We further identified a small number of members of this gene family as differentially expressed in female reproductive ovule tissues harbouring mature gametophytes from apomictic and sexual accessions. This included homologues of A. thaliana FASCIATED STEM 4 (FAS4) and of ENHANCED SILENCING PHENOTYPE 3 (ESP3), which have previously been identified as potential candidates for gametogenesis and apomixis, respectively. Unlike in A. thaliana, for either of them additional homologues or copies of related genes are present in Boechera, indicating complex evolutionary histories. As the expression patterns implied potential roles of FAS4 during gametogenesis, we first studied A. thaliana lines carrying mutant alleles. Indeed, we observed defects during male and female gametogenesis and severely reduced transmission efficiencies through both parents. In conclusion, our study identifies FAS4 as crucial for plant reproduction and suggests the potential for sub-functionalization of additional homologous genes in Boechera to shape reproductive development.

plant biology↗

Pharmacologic Stabilization of Retromer Rescues Endosomal Pathology Induced by Defects in the Alzheimer's gene SORL1

The Sortilin-related receptor 1 gene (SORL1, SORLA) is strongly associated with risk of developing Alzheimers disease (AD). SORLA is a regulator of endosomal trafficking in neurons and interacts with retromer, a complex that is a master conductor of endosomal trafficking. Pharmacological chaperones stabilize retromer in vitro, enhancing its function. Here we used an isogenic series of human induced pluripotent stem cell (hiPSC) lines with either one or two copies of SORL1 or harboring one copy of a SORL1 variant linked to increased risk for AD. We treated hiPSC-derived cortical neurons with the established retromer chaperone, TPT-260, and tested whether indicators of ADs defining endosomal, amyloid, and Tau pathologies were corrected. We observed that the degree of rescue by TPT-260 treatment varied, depending on the number of copies of functional SORL1 and which SORL1 variant was expressed. Using a disease-relevant preclinical model, our work illuminates how the SORL1-retromer pathway can be therapeutically harnessed.

neuroscience↗

mTOR inhibition enhances delivery and activity of antisense oligonucleotides in uveal melanoma cells

Uveal melanoma (UM) is the most common primary intraocular malignancy in adults. Due to a lack of effective treatments, patients with metastatic disease have a median survival time of 6-12 months. We recently demonstrated that the SAMMSON long non-coding RNA (lncRNA) is essential for uveal melanoma cell survival and that antisense oligonucleotide (ASO)-mediated silencing of SAMMSON impaired cell viability and tumor growth in vitro and in vivo. By screening a library of 2911 clinical stage compounds, we identified the mTOR inhibitor GDC-0349 to synergize with SAMMSON inhibition in UM. Mechanistic studies revealed that mTOR inhibition enhanced uptake and reduced lysosomal accumulation of lipid complexed SAMMSON ASOs, improving SAMMSON knockdown and further decreasing UM cell viability. We found mTOR inhibition to also enhance target knockdown in other cancer cell lines as well as normal cells when combined with lipid nanoparticle complexed or encapsulated ASOs or small interfering RNAs (siRNAs). Our results are relevant to nucleic acid treatment in general and highlight the potential of mTOR inhibition to enhance ASO and siRNA mediated target knockdown.

cancer biology↗

Phytochemical Nrf2 activator attenuates skeletal muscle mitochondrial dysfunction and impaired proteostasis in a preclinical model of musculoskeletal aging

Musculoskeletal dysfunction is an age-related syndrome associated with impaired mitochondrial function and proteostasis. However, few interventions have tested targeting two drivers of musculoskeletal decline. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor that stimulates transcription of cytoprotective genes and improves mitochondrial function. We hypothesized daily treatment with a Nrf2 activator in Hartley guinea pigs, a model of age-related musculoskeletal dysfunction, attenuates the progression of skeletal muscle mitochondrial dysfunction and impaired proteostasis, preserving musculoskeletal function. We treated 2-month- and 5-month-old male and female Hartley guinea pigs for 3 and 10 months, respectively, with the phytochemical Nrf2 activator PB125 (Nrf2a). Longitudinal assessments of voluntary mobility were measured using Any-Maze open-field enclosure monitoring. Cumulative skeletal muscle protein synthesis rates were measured using deuterium oxide over the final 30 days of treatment. Mitochondrial oxygen consumption in permeabilized soleus muscles was measured using ex vivo high resolution respirometry. In both sexes, Nrf2a 1) increased electron transfer system capacity; 2) attenuated the disease/age-related decline in coupled and uncoupled mitochondrial respiration; and 3) attenuated declines in protein synthesis in the myofibrillar, mitochondrial, and cytosolic subfractions of the soleus. These improvements were not associated with statistically significant prolonged maintenance of voluntary mobility in guinea pigs. Collectively, these results demonstrate that treatment with an oral Nrf2 activator contributes to maintenance of skeletal muscle mitochondrial function and proteostasis in a pre-clinical model of musculoskeletal decline. Further investigation is necessary to determine if these improvements are also accompanied by slowed progression of other aspects of musculoskeletal decline.

physiology↗

Robust linear modelling in ElectroEncephaloGraphy can be obtained using single weights reflecting each single trials' dynamics

Being able to remove or weigh down the influence of outlier data is desirable for any statistical models. While Magnetic and ElectroEncephaloGraphic (MEEG) data are often averaged across trials per condition, it is becoming common practice to use information from all trials to build statistical linear models. Individual trials can, however, have considerable weight and thus bias inferential results (effect sizes as well as thresholded t/F/p maps). Here, rather than looking for univariate outliers, defined independently at each measurement point, we apply the principal component projection (PCP) method at each channel, deriving a single weight per trial at each channel independently. Using both synthetic data and open EEG data, we show (1) that PCP is efficient at detecting a large variety of outlying trials; (2) how PCP-based weights can be implemented in the context of the general linear model (GLM) with accurate control of type 1 family-wise error rate; and (3) that our PCP-based Weighted Least Square (WLS) approach increases the statistical power of group analyses as well as a much slower Iterative Reweighted Least Squares (IRLS), although the weighting scheme is markedly different. Together, our results show that WLS based on PCP weights derived from whole trial profiles is an efficient method to weigh down the influence of outlier EEG data in linear models. Data availabilityall data used are publicly available (CC0), all code (simulations and data analyzes) is also available online in the LIMO MEEG GitHub repository (MIT license).

neuroscience↗