bluuebunny/crossref_metadata_2025_split huggingface dataset:
Air leaks: stapling affects porcine lungs biomechanics
Authors: Bonnet Bénédicte , Tabiai Ilyass , Rakovich George , Gosselin Frédérick P. , Villemure Isabelle 
Published: April 2021

AbstractDuring thoracic operations, surgical staplers resect cancerous tumors and seal the spared lung. However, post-operative air leaks are undesirable clinical consequences: staple legs wound lung tissue. Subsequent to this trauma, air leaks from lung tissue into the pleural space. This affects the lung’s physiology and patients’ recovery.The objective is to biomechanically and visually characterize porcine lung tissue with and without staples in order to gain knowledge on air leakage following pulmonary resection. Therefore, a syringe pump filled with air inflates and deflates eleven porcine lungs cyclically without exceeding 10 cmH2O of pressure. Cameras capture stereo-images of the deformed lung surface at regular intervals while a microcontroller simultaneously records the alveolar pressure and the volume of air pumped. The raw images are then used to compute tri-dimensional displacements and strains with the Digital Image Correlation method (DIC).Air bubbles originated at staple holes of inner row from exposed porcine lung tissue due to torn pleural on costal surface. Compared during inflation, left upper or lower lobe resections have similar compliance (slope of the pressure vs volume curve), which are 9% lower than healthy lung compliance. However, lower lobes statistically burst at lower pressures than upper lobes (p-value<0.046) inex vivoconditions confirming previous clinicalin vivostudies. In parallel, the lung deformed mostly in the vicinity of staple holes and presented maximum shear strain near the observed leak location. To conclude, a novel technique DIC provided concrete evidence of the post-operative air leaks biomechanics. Further studies could investigate causal relationships between the mechanical parameters and the development of an air leak.
Appetitive learning relies on octopamine and dopamine in ants
Authors: Wissink Maarten , Nehring Volker 
Published: April 2021

AbstractAssociative learning relies on the detection of coincidence between a stimulus and a reward or punishment. In the insect brain, this process is thought to be carried out in the mushroom bodies under control of octopaminergic and dopaminergic neurons. It was assumed that appetitive learning is governed by octopaminergic neurons, while dopamine is required for aversive learning. This view has been recently challenged: Both neurotransmitters seem to be involved in both types of memory in bees and flies. Here, we test which neurotransmitters are required for appetitive learning in ants. We trainedLasius nigerant workers to discriminate two mixtures of linear hydrocarbons and associate one of them with a sucrose reward. We analysed the behaviour of the trained ants using machine learning and found that they preferred the rewarded odour over the other, a preference that was stable for at least 24 hours. We then treated the ants before learning with either epinastine, an octopamine receptor blocker, or with flupentixol, a dopamine receptor blocker. Ants with blocked octopamine receptors did not remember the rewarded odour. Octopamine signalling is thus necessary for the formation of appetitive memory. In contrast, ants with blocked dopamine receptors initially learned the rewarded odour but failed to retrieve this memory 24 hours later. Dopamine is thus required for long-term memory consolidation during appetitive conditioning, independent of short-term memory formation. Our results show that appetitive learning depends on both octopamine and dopamine signalling in ants.
Cell division in tissues enables macrophage infiltration
Authors: Akhmanova Maria , Gyoergy Attila , Vlasov Mikhail , Vlasov Fedor , Krueger Daniel , Akopian Andrei , Emtenani Shamsi , Ratheesh Aparna , De Renzis Stefano , Siekhaus Daria E. 
Published: April 2021

AbstractMigration of cells through diverse tissues is essential for development, immune response and cancer metastasis1–3. To reach their destination, cells must overcome the resistance imposed by complex microenvironments, composed of neighboring cells and extracellular matrix (ECM)4–6. While migration through pores and tracks in ECM has been well studied4,5,7, little is known about cellular traversal into confining cell-dense tissues. Here by combining quantitative live imaging with genetic and optogenetic perturbations we identify a crucial role for cell division during cell migration into tissues. We find that normal embryonic invasion byDrosophilamacrophages between the ectoderm and mesoderm8,9absolutely requires division of an epithelial ectodermal cell at the site of entry. Dividing ectodermal cells disassemble ECM attachment formed by Integrin-mediated focal adhesions next to mesodermal cells, allowing macrophages to move their nuclei ahead and invade. Decreasing or increasing the frequency of ectodermal division correspondingly either hinders or promotes macrophage invasion. Reducing the levels of focal adhesion components in the ectoderm allows macrophage entry even in the absence of division. Our study demonstrates the critical importance of division at the entry site to enablein vivocell invasion by relieving the steric impediment caused by focal adhesions. We thus provide a new perspective on the regulation of cellular movement into tissues.
Brain structure-function coupling provides signatures for task decoding and individual fingerprinting
Authors: Griffa Alessandra , Amico Enrico , Liégeois Raphaël , Van De Ville Dimitri , Preti Maria Giulia 
Published: April 2021

AbstractBrain signaturesof functional activity have shown promising results in bothdecodingbrain states, meaning distinguishing between different tasks, andfingerprinting, that is identifying individuals within a large group. Importantly, these brain signatures do not account for the underlying brain anatomy on which brain function takes place. Structure-function coupling based on graph signal processing (GSP) has recently revealed a meaningful spatial gradient from unimodal to transmodal regions, on average in healthy subjects during resting-state. Here, we explore the potential of GSP to introduce new imaging-based biomarkers to characterize tasks and individuals. We used multimodal magnetic resonance imaging of 100 unrelated healthy subjects from the Human Connectome Project both during rest and seven different tasks and adopted a support vector machine classification approach for bothdecodingandfingerprinting, with various cross-validation settings. We found that structurefunction coupling measures allow accurate classifications for both task decoding and fingerprinting. In particular, key information for fingerprinting is found in the more liberal portion of functional signals, that is the one decoupled from structure. A network mainly involving cortico-subcortical connections showed the strongest correlation with cognitive traits, assessed with partial least square analysis, corroborating its relevance for fingerprinting. By introducing a new perspective on GSP-based signal filtering and FC decomposition, these results show that brain structure-function coupling provides a new class of signatures of cognition and individual brain organization at rest and during tasks. Further, they provide insights on clarifying the role of low and high spatial frequencies of the structural connectome, leading to new understanding of where key structure-function information for characterizing individuals can be found across the structural connectome graph spectrum.Highlights-The relation of brain function with the underlying structural wiring is complex-We propose new structure-informed graph signal processing (GSP) of functional data-GSP-derived features allow accurate task decoding and individual fingerprinting-Functional connectivity from filtered data is more unique to subject and cognition-The role of structurally aligned and liberal graph frequencies is elucidated
Improved post-stroke spontaneous recovery by astrocytic extracellular vesicles
Authors: Heras-Romero Yessica , Morales-Guadarrama Axayacatl , Santana-Martínez Ricardo , Ponce Isaac , Rincón-Heredia Ruth , Poot-Hernández Augusto César , Martínez-Moreno Araceli , Urrieta Esteban , Bernal-Vicente Berenice N. , Campero-Romero Aura N. , Moreno-Castilla Perla , Greig Nigel H. , Escobar Martha L. , Concha Luis , Tovar-y-Romo Luis B. 
Published: April 2021

AbstractSpontaneous recovery after a stroke accounts for a major part of the neurological recovery in patients. However limited, the spontaneous recovery is mechanistically driven by axonal restorative processes for which several molecular cues have been previously described. We report the acceleration of spontaneous recovery in a preclinical model of ischemia/reperfusion in rats via a single intracerebroventricular administration of extracellular vesicles released from primary cortical astrocytes. We used MRI, confocal and multiphoton microscopy to correlate the structural remodeling of the corpus callosum and striatocortical circuits with neurological performance over 21 days. We also evaluated the functionality of the corpus callosum by repetitive recordings of compound action potentials to show that the recovery facilitated by astrocytic extracellular vesicles was both anatomical and functional. Our data provide compelling evidence that astrocytes can hasten the basal recovery that naturally occurs post-stroke through the release of cellular mediators contained in extracellular vesicles.
Fibrin Prestress Due to Platelet Aggregation and Contraction Increases Clot Stiffness
Authors: Pathare Suyog J. , Eng Wilson , Lee Sang-Joon J. , Ramasubramanian Anand K. 
Published: April 2021

AbstractEfficient haemorrhagic control is attained through the formation of strong and stable blood clots at the site of injury. Although it is known that platelet-driven contraction can dramatically influence clot stiffness, the underlying mechanisms by which platelets assist fibrin networks in resisting external loads are not understood. In this study, we delineate the contribution of platelet-fibrin interactions to clot tensile mechanics using a combination of new mechanical measurements, image analysis, and structural mechanics simulation. Based on uniaxial tensile test data using custom-made microtensometer, and fluorescence microscopy of platelet aggregation and platelet-fibrin interactions, we show that integrin-mediated platelet aggregation and actomyosin-driven platelet contraction synergistically increase the elastic modulus of the clots. We demonstrate that the mechanical and geometric response of an active contraction model of platelet aggregates compacting vicinal fibrin is consistent with the experimental data. The model suggests that platelet contraction induces prestress in fibrin fibres, and increases the effective stiffness in both crosslinked and non-crosslinked clots. Our results provide evidence for fibrin compaction at discrete nodes as a major determinant of mechanical response to applied loads.
Surface residues and non-additive interactions stabilize a consensus homeodomain protein
Authors: Sternke Matt , Tripp Katherine W. , Barrick Doug 
Published: April 2021

AbstractDespite the widely reported success of consensus design in producing highly stabilized proteins, little is known about the physical mechanisms underlying this stabilization. Here we explore the potential sources of stabilization by performing a systematic analysis of the 29 substitutions that we previously found to collectively stabilize a consensus homeodomain compared to an extant homeodomain. By separately introducing groups of consensus substitutions that alter or preserve charge state, occur at varying degrees of residue burial, and occur at positions of varying degrees of conservation, we determine the extent to which these three features contribute to the consensus stability enhancement. Surprisingly, we find that the largest total contribution to stability comes from consensus substitutions on the protein surface and that the largest per-substitution contributions come from substitutions that maintain charge state, suggesting that although consensus proteins are often enriched in charged residues, consensus stabilization does not result primarily from charge-charge interactions. Although consensus substitutions at strongly conserved positions also contribute disproportionately to stabilization, significant stabilization is also contributed from substitutions at weakly conserved positions. Furthermore, we find that identical consensus substitutions show larger stabilizing effects when introduced into the consensus background than when introduced into an extant homeodomain, indicating that synergistic, stabilizing interactions among the consensus residues contribute to consensus stability enhancement of the homeodomain.Significance StatementProteins composed of consensus sequences from multiple sequence alignments are often more stable than extant proteins used to create them. Often about half the residues in a consensus protein differ from those of extant proteins. The contributions of these differences to stability are unknown. Here we substitute groups of residues with different properties (conservation, charge variation, solvent accessibility) to determine which substitutions lead to consensus stabilization. We find that surface and charge-conserving substitutions contribute to stability, that weakly-conserved substitutions make a significant collective contribution to stability, and that there is a significant non-additive contribution to stability in the consensus background. These results provide insights to the sequence origins of consensus stabilization and the evolutionary constraints that determine protein sequences.
Identifying Upper Airway and Evaluating Adenoid in Lateral Cephalometric Radiographs of Pediatric Patients Using Image-based Deep Learning Technique
Authors: Yao Kan , Xie Yilun , Yu Wenwen , Wei Silong , Xia Liang , Zheng Tong , Lu Xiaofeng 
Published: April 2021

AbstractPurposeAdenotonsillar hypertrophy is considered as one of the primary causes of pediatric obstructive sleep apnea. In clinical practice, pediatric patients with potential obstructive apnea should undergo assessment of upper airway obstruction and adenotonsillar size. As lack of well-trained physicians in China, large numbers of such patients could not be accurately evaluated in time. We attempted to find a better way to assess upper airway obstruction.MethodsWe developed a computational method which may allow clinicians to trace upper airway obstruction. We utilized a Detectron2 Mask R-CNN architecture that was pretrained on ImageNet-1k dataset. We then trained it on our COCO dataset using transfer learning for segmentations of upper airway and related key structures. With the instance segmentations, we utilized a tracing algorithm developed by our own to sketch the contours of key segments. At the end, our system would use the traced landmarks to calculate the targeted clinical data.ResultsWe validated the effective-ness of the algorithm in two steps. First, we used a validation set (COCO dataset) to evaluate the segmentation performance of our system. Our system achieved a mean segmentation AP of 61.30, with airway segmentation AP of 55.64 and cranial base segmentation AP of 66.96. In addition, the AP50was 99.49 and AP75was 73.62. Second,we analyzed the data from our system and experts using a single rater, absolute-agreement, 2-way mixed-effects model, and got ICC value of 0.73 with 95% confident interval = 0.63-0.81.ConclusionsIn this study, we created a deep-learning based system to help clinicians evaluate upper airway in lateral cephalometric radiographs which we believe could improve clinical practice. With the evolving of technology, our system would become more integrated into medical care of OSA, freeing the clinical practitioners from repetitive tasks and enabling them to concentrate on improved patient care.
Bone innervation and vascularization regulated by osteoclasts contribute to refractive pain-related behavior in the collagen antibody-induced arthritis model
Authors: Rudjito Resti , Agalave Nilesh M , Farinotti Alex Bersellini , Baharpoor Azar , Martinez Martinez Arisai , Islas Enriqueta Muñoz , Panwar Preety , Brömme Dieter , Barbier Julie , Marchand Fabien , Mehlen Patrick , Andersen Thomas Levin , Andrade Juan Miguel Jimenez , Svensson Camilla I. 
Published: April 2021

ABSTRACTObjectiveRheumatoid arthritis is often characterized by eroded joints and chronic pain that outlasts disease activity. Whilst several reports show strong associations between bone resorption and nociception, the underlying mechanisms remain to be unraveled. Here, we used the collagen antibody-induced arthritis (CAIA) model to examine the contribution of osteoclasts in pain regulation. The antinociceptive effects of osteoclasts inhibitors and their mechanisms of actions involving bone vascularization and innervation were also explored.MethodsBALB/c female mice were subjected to CAIA by intravenous injection of a collagen type-II antibody cocktail, followed by intraperitoneal injection of lipopolysaccharide. Degree of arthritis, bone resorption, mechanical hypersensitivity, vascularization and innervation in the ankle joint were assessed. Animals were treated with osteoclast inhibitors, zoledronate and cathepsin K inhibitor (T06), and netrin-1 neutralizing antibody. Potential pronociceptive factors were examined in primary osteoclast cultures.ResultsCAIA induced local bone loss in the calcaneus with ongoing increased osteoclast activity during the inflammatory phase of the model, but not after inflammation has resolved. Mechanical hypersensitivity was reversed by zoledronate in late but not inflammatory phase CAIA. This effect was coupled to the ability of osteoclasts to modulate bone vascularization and innervation, which was inhibited by osteoclast inhibitors. CAIA-induced hypersensitivity in the late phase was also reversed by anti-netrin-1 antibody.ConclusionOsteoclasts induce pain-like behavior in the CAIA model independent of inflammation via effects on bone vascularization and innervation.Key messagesWhat is already known about this subject?Pain and residual signs of erosive lesions are frequently present in rheumatoid arthritis (RA) patients with good disease controlOsteoclasts can induce nociceptive signaling but the exact mechanism with respect to RA-induced pain is not clearWhat does this study add?The pronociceptive actions of osteoclasts extend beyond flares of joint inflammation and erosive activity by increasing bone innervation, bone vascularization and netrin-1 releaseOsteoclast inhibitors and neutralizing netrin-1 antibodies reverse refractive pain-related behaviors in the collagen antibody-induced arthritis modelHow might this impact on clinical practice or future developments?This study provides insights to the potential of osteoclast inhibition as a therapeutic strategy for persistent pain in RA
A pilot study to define and identify future priorities intoAllocasuarina robustarecovery as part of a community program
Authors: Pearson Matthew W 
Published: April 2021

AbstractTheAllocasuarina robustapilot study investigated the process involved to facilitate seed recruitment as part of a threatened species project. Several experiments occurred, each examining a specific attribute in the seed recruitment process.A. robustais a threatened species of national and local significance. The research design would help land managers and communities to conserveA. robusta. The investigation aimed to improve seed recruitment inA. robustaoccurring under natural conditions. The experiment results highlighted several experimental design flaws and identified opportunities to increase community participation as part of the recovery program.
Age-dependent genetic architecture underlines similar heritability of body size in sticklebacks
Authors: Fraimout Antoine , Li Zitong , Sillanpää Mikko J. , Merilä Juha 
Published: April 2021

AbstractHeritable variation in traits under natural selection is a prerequisite for evolutionary response. While it is recognised that trait heritability may vary spatially and temporally depending under which environmental conditions traits are expressed, less is known about the possibility that genetic variance contributing to the expected selection response in a given trait may vary at different stages of ontogeny. Specifically, whether different loci underlie the expression of a trait throughout development – thus providing an additional source of variation for selection to act on – is unclear. Here we show that the heritability (h2) of body size, an important life history trait, remains constant across ontogeny in a stickleback fish. Nevertheless, both analyses of quantitative trait loci (QTL) and genetic correlations across ages show that different chromosomes/loci contribute to this heritability in different ontogenic time-points. This suggests that body size can respond to selection at different stages of ontogeny but that this response is determined by different loci at different points of development. Hence, this illustrates the notion that diverse genetic architectures may underline similar (expected) phenotypic outcomes, and that similar selection pressures may lead to genetically heterogeneous responses depending on what life stage selection is acting on.
Active Rheumatoid Arthritis in a Mouse Model is not an Independent Risk Factor for Periprosthetic Joint Infection
Authors: Trikha Rishi , Greig Danielle , Sekimura Troy , Cevallos Nicolas , Kelley Benjamin , Mamouei Zeinab , Hart Christopher , Ralston Micah , Turkmani Amr , Sassoon Adam , Stavrakis Alexandra , Bernthal Nicholas M 
Published: April 2021

AbstractIntroductionPeriprosthetic joint infection (PJI) represents a devastating complication of total joint arthroplasty associated with significant morbidity and mortality. Literature suggests a possible higher incidence of periprosthetic joint infection (PJI) in patients with rheumatoid arthritis (RA). There is, however, no consensus on this relative risk nor a well-defined mechanism of this purported risk. This study investigates how collagen-induced arthritis (CIA), a validated animal model of RA, impacts infectious burden in a well-established model of PJI.MethodsControl mice were compared against CIA mice. Whole blood samples were collected to quantify systemic IgG levels via ELISA.Ex vivorespiratory burst function was measured via dihydrorhodamine assay.Ex vivo Staphylococcus aureusXen36 burden was measured directly via colony forming unit (CFU) counts and crystal violet assay to assess biofilm formation.In vivo, surgical placement of a titanium implant through the knee joint and inoculation withS. aureusXen36 was performed. Bacterial burden was then quantified by longitudinal bioluminescent imaging.ResultsMice with CIA demonstrated significantly higher levels of systemic IgG compared with control mice (p = 0.003).Ex vivo, there was no significant difference in respiratory burst function (p=0.89) orS. aureusbacterial burden as measured by CFU counts (p=0.91) and crystal violet assay (p=0.96).In vivo, no significant difference in bacterial bioluminescence between groups was found at all postoperative time points. CFU counts of both the implant and the peri-implant tissue were not significantly different between groups (p=0.82 and 0.80, respectively).ConclusionThis study demonstrated no significant difference inS. aureusinfectious burden between mice with CIA and control mice. These results suggest that untreated, active RA may not represent a significant intrinsic risk factor for PJI. Further mechanistic translational and clinical studies are, however, warranted to thoroughly investigate the infectious risk of RA.