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Biology subjects

Wood, E.

Publications and source records attributed to Wood, E..

10 recordsLinked to original sources

Local interaction networks reconstructed from global biodiversity data improve pollinator restoration decision making

Global pollinator declines threaten the health of ecosystems and food systems, underscoring the urgency of conservation actions such as habitat restoration. However, data gaps on plant use among pollinators continue to limit reliable design of restoration plant mixes. To address this, we present NECTAR (Network-Enhanced Conservation Tool for Analysis and Recommendation), a new modular framework that integrates multiple data modalities - including species distributions, phenological metrics, and phylogenetic data - to infer flower visitation and host plant interactions from spatial, temporal, and phylogenetic overlap, generating spatially explicit plant-insect interaction networks that guide planting recommendations for pollinator habitat restoration. We demonstrate the utility of NECTAR by generating a large plant-insect metaweb across California, comprising 2,473,729 spatially explicit interactions that included 3,792 pollinator species and 4,363 native plant species. NECTAR achieved high interaction recall across withheld interactions and independent datasets, substantially outperforming null models and matching or exceeding values reported in comparable studies. NECTAR's data-driven plant mix recommendations are predicted to support up to 2.4 times more pollinator species compared to existing resources and random selection of plants. This optimization facilitates the inclusion of multiple goals and constraints, and provides complementary decision-making information to existing resources. NECTAR offers a scalable, evidence-based framework for translating increasingly available global biodiversity data into locally actionable restoration guidance, with broad potential to improve pollinator habitat restoration worldwide.

ecology↗

Potential risk for hearing from prolonged exposure to sound at conversation levels

Prolonged exposure to loud and moderate noise impairs hearing; the lower the noise level, the lower risk of hearing loss is. To date, little is known about how low the noise level can be safe to hearing. This study investigated the risk of exposure to tone at typical conversational levels by measuring auditory brainstem response (ABR). We show that exposing C57 mice to continuous pure tone at 65 dB SPL for 1 hour (TE65) leads to an increase in ABR threshold that is specific to the exposure frequency. Tone exposure also increased the latencies and decreased the amplitude in Waves I and II but not in Waves III and V. Significantly, the changes in amplitude and latency were highly correlated in Wave I and such correlation gradually degraded from Wave I through to Wave V. Our findings suggest that exposure to low level sound can impair hearing and alter the auditory information process in the brain if it is persistent and presented over a sufficient period of time. Significant StatementOur findings established the risk of hearing impairment following the exposure to continuous tone at normal or conversational voice levels. This finding challenges current public health guidelines for hearing protection. Although further clarification is required, our studies prompt that the regular use of ABR testing is a potential protocol for diagnosing hearing impairment in patients experiencing hidden hearing loss (HHL).

neuroscience↗

Reduced Auditory Perception and Brain Response with Quiet TMS Coil

BACKGROUNDElectromagnetic forces in transcranial magnetic stimulation (TMS) coils generate a loud clicking sound that produces confounding auditory activation and is potentially hazardous to hearing. To reduce this noise while maintaining stimulation efficiency similar to conventional TMS coils, we previously developed a quiet TMS double containment coil (qTMS-DCC). OBJECTIVETo compare the stimulation strength, perceived loudness, and EEG response between qTMS-DCC and a commercial TMS coil. METHODSNine healthy volunteers participated in a within-subject study design. The resting motor thresholds (RMTs) for qTMS-DCC and MagVenture Cool-B65 were measured. Psychoacoustic titration matched the Cool-B65 loudness to qTMS-DCC pulsed at 80, 100, and 120% RMT. Event-related potentials (ERPs) were recorded for both coils. The psychoacoustic titration and ERPs were acquired with the coils both on and 6 cm off the scalp, the latter isolating the effects of airborne auditory stimulation from body sound and electromagnetic stimulation. The ERP comparisons focused on a centro-frontal region that encompassed peak responses in the global signal. RESULTSRMT did not differ significantly between the coils, with or without the EEG cap on the head. qTMS-DCC was perceived to be substantially quieter than Cool-B65. For example, qTMS-DCC at 100% coil-specific RMT sounded like Cool-B65 at 34% RMT. The general ERP waveform and topography were similar between the two coils, as were early-latency components, indicating comparable electromagnetic brain stimulation in the on-scalp condition. qTMS-DCC had a significantly smaller P180 component in both on-scalp and off-scalp conditions, supporting reduced auditory activation. CONCLUSIONSThe stimulation efficiency of qTMS-DCC matched Cool-B65, while having substantially lower perceived loudness and auditory-evoked potentials. HighlightsO_LIqTMS coil is subjectively and objectively quieter than conventional Cool-B65 coil C_LIO_LIqTMS coil at 100% motor threshold was as loud as Cool-B65 at 34% motor threshold C_LIO_LIAttenuated coil noise reduced auditory N100 and P180 evoked response components C_LIO_LIqTMS coil enables reduction of auditory activation without masking C_LI

bioengineering↗

Cell state transition analysis identifies interventions that improve control of M. tuberculosis infection by susceptible macrophages

Understanding cell state transitions and purposefully controlling them to improve therapies is a longstanding challenge in biological research and medicine. Here, we identify a transcriptional signature that distinguishes activated macrophages from TB-susceptible and TB-resistant mice. We then apply the cSTAR (cell State Transition Assessment and Regulation) approach to data from screening-by-RNA sequencing to identify chemical perturbations that shift the. transcriptional state of the TB-susceptible macrophages towards that of TB-resistant cells. Finally, we demonstrate that the compounds identified with this approach enhance resistance of the TB-susceptible mouse macrophages to virulent M. tuberculosis.

immunology↗

Adenovirus 14p1 induced changes in miRNA expression increases lung immunopathogenesis

Adenovirus is a frequent cause of mild, usually self-limited infections in infants and young children. Severe infections occur in immunocompromised patients but are rarely observed in healthy, immunocompetent adults. However, there have been outbreaks around the world of infections with different adenoviral (Ad) serotypes that have resulted in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) in some of those infected. Ad14p1, the predominant circulating strain of Ad14 worldwide is one such serotype. The explanations for the severity of illness caused by Ad14p1 infection in immunocompetent patients is unknown. Previously, we have shown that A549 cells infected with Ad14 repress macrophage pro29 inflammatory responses whereas cells infected with Ad14p1 fail to repress macrophages and, instead, can increase pro-inflammatory responses. Micro-RNAs (miRNA) are small noncoding RNAs that regulate gene expression at the posttranscriptional level. Adenoviral infection has been shown to modulate host miRNA expression, and we hypothesized that differences in miRNA expression between Ad14 and Ad14p1 infected cells might impact pathogenesis. A549 cells were infected with either Ad14 or Ad14p1 and total RNA samples were collected at 6, 12, 24, 36 and 48 post infection for miRNA sequencing. Cluster analysis revealed that there were 3 temporal changes in miRNA expression profiles following infection. Differential expression analysis showed 8-23 differentially expressed miRNA between Ad14 and Ad14p1 from 6 to 36hpi. However, at 48hpi there were 98 differentially expressed miRNAs in Ad14p1 infected cells compared to those infected by Ad14. Pathway enrichment analysis showed that the differentially expressed miRNA might explain the increased pathogenesis of Ad14p1caused by strain-related loss of modulation of cytokine expression. Overall, the data suggest a role for viral regulation of host miRNA expression in pathogenesis by regulating host inflammatory responses through the delivery of deregulated miRNAs by virally infected cell corpses to macrophages. Author SummaryAcute respiratory distress syndrome (ARDS) is a severe inflammatory disease in the lungs, and both the onset and resolution of ARDS appears to be regulated primarily by alveolar macrophages. Emergent strains of human adenovirus (Ad) can induce ARDS in healthy immunocompetent people, whereas most, common Ad infections go unnoticed or causes minimal symptoms. Why emergent strains of Ad, such as Ad14p1, are more likely to induce acute lung injury (ALI) and ARDS is unknown. Cells that die from wild type Ad14 infection have been shown to repress alveolar macrophage inflammatory responses, whereas cells dying from Ad14p1 infection enhance inflammatory responses of alveolar macrophages. Here, we explored whether virus induced changes in the expression of cellular small regulatory RNAs could explain the differential effects of virally infected cells on alveolar macrophage inflammatory responses. The data show that there are differences in small RNA expression between Ad14 and Ad14p1 infected cells at late times after infection, when Ad14p1 infected cells lose expression of the small RNAs that repress pro-inflammatory cellular signaling pathways in macrophages. Our study provides insights into a mechanism that could drive the increased pathogenesis of some outbreak strains of adenovirus.

microbiology↗

TAP: Targeting and analysis pipeline for optimization and verification of TMS coil placement

ObjectiveTranscranial magnetic stimulation (TMS) can modulate brain function via an electric field (E-field) induced in a region of interest (ROI) in the brain. The ROI E-field can be computationally maximized and set to match a specific reference using individualized head models to find the optimal coil placement and stimulus intensity. However, the available software lacks many practical features for prospective planning of TMS interventions and retrospective evaluation of the experimental targeting accuracy. ApproachThe TMS targeting and analysis pipeline (TAP) software uses an MRI/fMRI-derived brain target to optimize coil placement considering experimental parameters such as the subjects hair thickness and coil placement restrictions. The coil placement optimization is implemented in SimNIBS 3.2, for which an additional graphical user interface (TargetingNavigator) is provided to visualize and adjust procedural parameters. The coil optimization process also computes the E-field at the target, allowing the selection of the TMS device intensity setting to achieve a specific E-field strength. The optimized coil placement information is prepared for neuronavigation software, which supports targeting during the TMS procedure. The neuronavigation system can record the coil placement during the experiment, and these data can be processed in TAP to quantify the accuracy of the experimental TMS coil placement and induced E-field. Main resultsTAP was demonstrated in a study consisting of three repetitive TMS sessions in five subjects. TMS was delivered by an experienced operator under neuronavigation with the computationally optimized coil placement. Analysis of the experimental accuracy from the recorded neuronavigation data indicated coil location and orientation deviations up to about 2 mm and 2{degrees}, respectively, resulting in an 8% median decrease in the target E-field magnitude compared to the optimal placement. SignificanceTAP supports navigated TMS with a variety of features for rigorous and reproducible stimulation delivery, including planning and evaluation of coil placement and intensity selection for E-field-based dosing.

neuroscience↗

Analogue representation of a spatial memory by ramp-like neural activity in retrohippocampal cortex

Neurons in the retrohippocampal cortices play crucial roles in spatial memory. Many retrohippocampal neurons have firing fields that are selectively active at specific locations, with memory for rewarded locations associated with reorganisation of these firing fields. Whether this is the sole strategy for representing spatial memories is unclear. Here, we demonstrate that during a spatial memory task retrohippocampal neurons encode location through ramping activity that extends within segments of a linear track approaching and following a reward, with the rewarded location represented by offsets or switches in the slope of the ramping activity. These ramping representations could be maintained independently of trial outcome and cues that mark the reward location, indicating that they result from recall of the track structure. During recordings in an open arena, neurons that generated ramping activity during the spatial memory task were more numerous than grid or border cells, with a majority showing spatial firing that did not meet criteria for classification as grid or border representations. Encoding of rewarded locations through offsets and switches in the slope of ramping activity also emerged in recurrent neural networks trained to solve a similar location memory task. Impaired performance of these networks following disruption of outputs from ramping neurons is consistent with this coding strategy supporting navigation to recalled locations of behavioural significance. We hypothesise that retrohippocampal ramping activity mediates readout of learned models for goal-directed navigation.

neuroscience↗

Syntax-sensitive regions of Broca's area and the posterior temporal lobe are differentially recruited by production and perception

Neuroimaging studies of syntactic processing typically result in similar activation profiles in Brocas area and the posterior temporal lobe (PTL). However, substantial functional dissociations between these regions have been demonstrated with respect to lesion-symptom mapping in aphasia. To account for this, Matchin & Hickok (2020) proposed that both regions play a role in syntactic processing, broadly construed, but attribute distinct functions to these regions with respect to production and comprehension. Here we report an fMRI study designed to test this hypothesis by contrasting the subvocal articulation and comprehension of structured jabberwocky phrases (syntactic), sequences of real words (lexical), and sequences of pseudowords (phonological). We defined two sets of language-selective regions of interest (ROIs) in individual subjects for Brocas area and the PTL using the contrasts [syntactic > lexical] and [syntactic > phonological]. We found robust significant interactions of comprehension and production between these two regions at the syntactic level, for both sets of language-selective ROIs. This suggests a core difference in the function of these regions: language-selective subregions of Brocas area play a role in syntax driven by the demands of production, whereas language-selective subregions of the PTL play a role in syntax driven by the demands of comprehension.

neuroscience↗

Myeloid-secreted BDNF maintains innervation of inguinal adipose in male mice

BackgroundInnervation of adipose tissue is essential for the proper function of this critical metabolic organ. Numerous surgical and chemical denervation studies have demonstrated how maintenance of brain-adipose communication through both sympathetic efferent and sensory afferent nerves helps regulate adipocyte size, cell number, lipolysis, and browning of white adipose tissue. Neurotrophic factors are growth factors that promote neuron survival, regeneration and plasticity, including neurite outgrowth and synapse formation. Peripheral blood immune cells have been shown to be a source of neurotrophic factors in humans and mice. Although a number of immune cells reside in the adipose stromal vascular fraction (SVF), it has remained unclear what roles they play in adipose innervation. We previously demonstrated that adipose immune cells secrete brain derived neurotrophic factor (BDNF). MethodsWe now show that deletion of this neurotrophic factor from the myeloid lineage led to a genetic denervation of inguinal subcutaneous white adipose tissue (scWAT), thereby causing decreased energy expenditure, increased adipose mass, and a blunted UCP1 response to cold stimulation. ResultsWe and others have previously shown that noradrenergic stimulation via cold exposure increases adipose innervation in the inguinal depot. Here we have identified a subset of myeloid cells that home to scWAT upon cold exposure and are Ly6C + CCR2 + Cx3CR1 + monocytes/macrophages that express noradrenergic receptors and BDNF. ConclusionsWe propose that these cold induced neuroimmune cells (CINCs) are key players in maintaining adipose innervation as well as promoting adipose nerve remodeling under noradrenergic stimulation, such as cold exposure.

neuroscience↗

Clinical long-read sequencing of the human mitochondrial genome for mitochondrial disease diagnostics

PurposeLong-read, third generation, sequencing technologies have the potential to improve current state of the art diagnostic strategies. In order to determine if long-read sequencing technologies are suitable for the diagnosis of mitochondrial disorders due to mitochondrial DNA (mtDNA) variants, particularly large deletions, we compared the performance of Oxford Nanopore Technologies (ONT) MinION to current diagnostic methods.\n\nMethodsWe sequenced mtDNA from nine patients with mtDNA deletion disorders and three normal controls with both ONT MinION and Illumina MiSeq. We applied a computational pipeline to estimate the positions of mtDNA deletions in patients, and subsequently validated the breakpoints using Sanger sequencing.\n\nResultsWe were able to detect mtDNA deletions with a MinION workflow, successfully calling the disease causing event in all cases. Sequencing coverage was in most cases significantly more (p=0.03, Wilcoxon test) uniform with MinION than with MiSeq and subsequent correction of MinION reads improved breakpoint accuracy and reduced false positives. Although heteroplasmic single nucleotide variants are detectable, the high number of false positives and false negatives precludes their use in diagnostics at this time.\n\nConclusionThe MinION is becoming an increasingly attractive diagnostic tool due to the reducing cost, increasing accuracy, and the speed at which data can be obtained.

genomics↗