334 research outputs found
Active Vibration Fluidization for Granular Jamming Grippers
Granular jamming has recently become popular in soft robotics with widespread
applications including industrial gripping, surgical robotics and haptics.
Previous work has investigated the use of various techniques that exploit the
nature of granular physics to improve jamming performance, however this is
generally underrepresented in the literature compared to its potential impact.
We present the first research that exploits vibration-based fluidisation
actively (e.g., during a grip) to elicit bespoke performance from granular
jamming grippers. We augment a conventional universal gripper with a
computer-controllled audio exciter, which is attached to the gripper via a 3D
printed mount, and build an automated test rig to allow large-scale data
collection to explore the effects of active vibration. We show that vibration
in soft jamming grippers can improve holding strength. In a series of studies,
we show that frequency and amplitude of the waveforms are key determinants to
performance, and that jamming performance is also dependent on temporal
properties of the induced waveform. We hope to encourage further study focused
on active vibrational control of jamming in soft robotics to improve
performance and increase diversity of potential applications.Comment: arXiv admin note: substantial text overlap with arXiv:2109.1049
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Autophagy gene haploinsufficiency drives chromosome instability, increases migration, and promotes early ovarian tumors.
Autophagy, particularly with BECN1, has paradoxically been highlighted as tumor promoting in Ras-driven cancers, but potentially tumor suppressing in breast and ovarian cancers. However, studying the specific role of BECN1 at the genetic level is complicated due to its genomic proximity to BRCA1 on both human (chromosome 17) and murine (chromosome 11) genomes. In human breast and ovarian cancers, the monoallelic deletion of these genes is often co-occurring. To investigate the potential tumor suppressor roles of two of the most commonly deleted autophagy genes in ovarian cancer, BECN1 and MAP1LC3B were knocked-down in atypical (BECN1+/+ and MAP1LC3B+/+) ovarian cancer cells. Ultra-performance liquid chromatography mass-spectrometry metabolomics revealed reduced levels of acetyl-CoA which corresponded with elevated levels of glycerophospholipids and sphingolipids. Migration rates of ovarian cancer cells were increased upon autophagy gene knockdown. Genomic instability was increased, resulting in copy-number alteration patterns which mimicked high grade serous ovarian cancer. We further investigated the causal role of Becn1 haploinsufficiency for oncogenesis in a MISIIR SV40 large T antigen driven spontaneous ovarian cancer mouse model. Tumors were evident earlier among the Becn1+/- mice, and this correlated with an increase in copy-number alterations per chromosome in the Becn1+/- tumors. The results support monoallelic loss of BECN1 as permissive for tumor initiation and potentiating for genomic instability in ovarian cancer
Orientational Melting in Carbon Nanotube Ropes
Using Monte Carlo simulations, we investigate the possibility of an
orientational melting transition within a "rope" of (10,10) carbon nanotubes.
When twisting nanotubes bundle up during the synthesis, orientational
dislocations or twistons arise from the competition between the anisotropic
inter-tube interactions, which tend to align neighboring tubes, and the torsion
rigidity that tends to keep individual tubes straight. We map the energetics of
a rope containing twistons onto a lattice gas model and find that the onset of
a free "diffusion" of twistons, corresponding to orientational melting, occurs
at T_OM > 160 K.Comment: 4 page LaTeX file with 3 figures (10 PostScript files
Quantum Monte Carlo calculation of Compton profiles of solid lithium
Recent high resolution Compton scattering experiments in lithium have shown
significant discrepancies with conventional band theoretical results. We
present a pseudopotential quantum Monte Carlo study of electron-electron and
electron-ion correlation effects on the momentum distribution of lithium. We
compute the correlation correction to the valence Compton profiles obtained
within Kohn-Sham density functional theory in the local density approximation
and determine that electronic correlation does not account for the discrepancy
with the experimental results. Our calculations lead do different conclusions
than recent GW studies and indicate that other effects (thermal disorder,
core-valence separation etc.) must be invoked to explain the discrepancy with
experiments.Comment: submitted to Phys. Rev.
Moderate hypoxia induces metabolic divergence in circulating monocytes and tissue resident macrophages from Berkeley sickle cell anemia mice
IntroductionHuman and murine sickle cell disease (SCD) associated pulmonary hypertension (PH) is defined by hemolysis, nitric oxide depletion, inflammation, and thrombosis. Further, hemoglobin (Hb), heme, and iron accumulation are consistently observed in pulmonary adventitial macrophages at autopsy and in hypoxia driven rodent models of SCD, which show distribution of ferric and ferrous Hb as well as HO-1 and ferritin heavy chain. The anatomic localization of these macrophages is consistent with areas of significant vascular remodeling. However, their contributions toward progressive disease may include unique, but also common mechanisms, that overlap with idiopathic and other forms of pulmonary hypertension. These processes likely extend to the vasculature of other organs that are consistently impaired in advanced SCD.MethodsTo date, limited information is available on the metabolism of macrophages or monocytes isolated from lung, spleen, and peripheral blood in humans or murine models of SCD.ResultsHere we hypothesize that metabolism of macrophages and monocytes isolated from this triad of tissue differs between Berkley SCD mice exposed for ten weeks to moderate hypobaric hypoxia (simulated 8,000 ft, 15.4% O2) or normoxia (Denver altitude, 5000 ft) with normoxia exposed wild type mice evaluated as controls.DiscussionThis study represents an initial set of data that describes the metabolism in monocytes and macrophages isolated from moderately hypoxic SCD mice peripheral lung, spleen, and blood mononuclear cells
Sulfide geochronology along the Endeavour Segment of the Juan de Fuca Ridge
Forty-nine hydrothermal sulfide-sulfate rock samples from the Endeavour Segment of the Juan de Fuca Ridge, northeastern Pacific Ocean, were dated by measuring the decay of 226Ra (half-life of 1600 years) in hydrothermal barite to provide a history of hydrothermal venting at the site over the past 6000 years. This dating method is effective for samples ranging in age from âŒ200 to 20,000 years old and effectively bridges an age gap between shorter- and longer-lived U-series dating techniques for hydrothermal deposits. Results show that hydrothermal venting at the active High Rise, Sasquatch, and Main Endeavour fields began at least 850, 1450, and 2300 years ago, respectively. Barite ages of other inactive deposits on the axial valley floor are between âŒ1200 and âŒ2200 years old, indicating past widespread hydrothermal venting outside of the currently active vent fields. Samples from the half-graben on the eastern slope of the axial valley range in age from âŒ1700 to âŒ2925 years, and a single sample from outside the axial valley, near the westernmost valley fault scarp is âŒ5850â±â205 years old. The spatial relationship between hydrothermal venting and normal faulting suggests a temporal relationship, with progressive younging of sulfide deposits from the edges of the axial valley toward the center of the rift. These relationships are consistent with the inward migration of normal faulting toward the center of the valley over time and a minimum age of onset of hydrothermal activity in this region of 5850 years
The distribution of radioactive 44Ti in Cassiopeia A
The distribution of elements produced in the innermost layers of a supernova explosion is a key diagnostic for studying the collapse of massive stars. Here we present the results of a 2.4 Ms NuSTAR observing campaign aimed at studying the supernova remnant Cassiopeia A (Cas A). We perform spatially resolved spectroscopic analyses of the 44Ti ejecta, which we use to determine the Doppler shift and thus the three-dimensional (3D) velocities of the 44Ti ejecta. We find an initial 44Ti mass of (1.54 ± 0.21) Ă 10â4 Mâ, which has a present-day average momentum direction of 340° ± 15° projected onto the plane of the sky (measured clockwise from celestial north) and is tilted by 58° ± 20° into the plane of the sky away from the observer, roughly opposite to the inferred direction of motion of the central compact object. We find some 44Ti ejecta that are clearly interior to the reverse shock and some that are clearly exterior to it. Where we observe 44Ti ejecta exterior to the reverse shock we also see shock-heated iron; however, there are regions where we see iron but do not observe 44Ti. This suggests that the local conditions of the supernova shock during explosive nucleosynthesis varied enough to suppress the production of 44Ti by at least a factor of two in some regions, even in regions that are assumed to be the result of processes like α-rich freezeout that should produce both iron and titanium
IL4Rα signaling abrogates hypoxic neutrophil survival and limits acute lung injury responses <i>in vivo</i>
Rationale: Acute respiratory distress syndrome is defined by the presence of systemic hypoxia and consequent on disordered neutrophilic inflammation. Local mechanisms limiting the duration and magnitude of this neutrophilic response remain poorly understood. Objectives: To test the hypothesis that during acute lung inflammation tissue production of proresolution type 2 cytokines (IL-4 and IL-13) dampens the proinflammatory effects of hypoxia through suppression of HIF-1a (hypoxia-inducible factor-1a)mediated neutrophil adaptation, resulting in resolution of lung injury. Methods: Neutrophil activation of IL4Ra (IL-4 receptor a) signaling pathways was explored ex vivo in human acute respiratory distress syndrome patient samples, in vitro after the culture of human peripheral blood neutrophils with recombinant IL-4 under conditions of hypoxia, and in vivo through the study of IL4Ra-deficient neutrophils in competitive chimera models and wild-type mice treated with IL-4. Measurements and Main Results: IL-4 was elevated in human BAL from patients with acute respiratory distress syndrome, and its receptor was identified on patient blood neutrophils. Treatment of human neutrophils with IL-4 suppressed HIF-1a-dependent hypoxic survival and limited proinflammatory transcriptional responses. Increased neutrophil apoptosis in hypoxia, also observed with IL-13, required active STAT signaling, and was dependent on expression of the oxygen-sensing prolyl hydroxylase PHD2. In vivo, IL-4Ra-deficient neutrophils had a survival advantage within a hypoxic inflamed niche; in contrast, inflamed lung treatment with IL-4 accelerated resolution through increased neutrophil apoptosis. Conclusions: We describe an important interaction whereby IL4Ra-dependent type 2 cytokine signaling can directly inhibit hypoxic neutrophil survival in tissues and promote resolution of neutrophil-mediated acute lung injury
Protection against glucose-induced neuronal death by NAAG and GCP II inhibition is regulated by mGluR3
Glutamate carboxypeptidase II (GCP II) inhibition has previously been shown to be protective against long-term neuropathy in diabetic animals. In the current study, we have determined that the GCP II inhibitor 2-(phosphonomethyl) pentanedioic acid (2-PMPA) is protective against glucose-induced programmed cell death (PCD) and neurite degeneration in dorsal root ganglion (DRG) neurons in a cell culture model of diabetic neuropathy. In this model, inhibition of caspase activation is mediated through the group II metabotropic glutamate receptor, mGluR3. 2-PMPA neuroprotection is completely reversed by the mGluR3 antagonist (S)-α-ethylglutamic acid (EGLU). In contrast, group I and III mGluR inhibitors have no effect on 2-PMPA neuroprotection. Furthermore, we show that two mGluR3 agonists, the direct agonist (2 R ,4 R )-4-aminopyrrolidine-2, 4-dicarboxylate (APDC) and N -acetyl-aspartyl-glutamate (NAAG) provide protection to neurons exposed to high glucose conditions, consistent with the concept that 2-PMPA neuroprotection is mediated by increased NAAG activity. Inhibition of GCP II or mGluR3 may represent a novel mechanism to treat neuronal degeneration under high-glucose conditions.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65724/1/j.1471-4159.2003.02321.x.pd
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