16 research outputs found
Performance capabilities of a JPL dual-arm advanced teleoperation system
The system comprises: (1) two PUMA 560 robot arms, each equipped with the latest JPL developed smart hands which contain 3-D force/moment and grasp force sensors; (2) two general purpose force reflecting hand controllers; (3) a NS32016 microprocessors based distributed computing system together with JPL developed universal motor controllers; (4) graphics display of sensor data; (5) capabilities for time delay experiments; and (6) automatic data recording capabilities. Several different types of control modes are implemented on this system using different feedback control techniques. Some of the control modes and the related feedback control techniques are described, and the achievable control performance for tracking position and force trajectories are reported. The interaction between position and force trajectory tracking is illustrated. The best performance is obtained by using a novel, task space error feedback technique
Impact of end effector technology on telemanipulation performance
Generic requirements for end effector design are briefly summarized as derived from generic functional and operational requirements. Included is a brief summary of terms and definitions related to end effector technology. The second part contains a brief overview of end effector technology work as JPL during the past ten years, with emphasis on the evolution of new mechanical, sensing and control capabilities of end effectors. The third and major part is devoted to the description of current end effector technology. The ongoing work addresses mechanical, sensing and control details with emphasis on mechanical ruggedness, increased resolution in sensing, and close electronic and control integration with overall telemanipulator control system
A laboratory breadboard system for dual-arm teleoperation
The computing architecture of a novel dual-arm teleoperation system is described. The novelty of this system is that: (1) the master arm is not a replica of the slave arm; it is unspecific to any manipulator and can be used for the control of various robot arms with software modifications; and (2) the force feedback to the general purpose master arm is derived from force-torque sensor data originating from the slave hand. The computing architecture of this breadboard system is a fully synchronized pipeline with unique methods for data handling, communication and mathematical transformations. The computing system is modular, thus inherently extendable. The local control loops at both sites operate at 100 Hz rate, and the end-to-end bilateral (force-reflecting) control loop operates at 200 Hz rate, each loop without interpolation. This provides high-fidelity control. This end-to-end system elevates teleoperation to a new level of capabilities via the use of sensors, microprocessors, novel electronics, and real-time graphics displays. A description is given of a graphic simulation system connected to the dual-arm teleoperation breadboard system. High-fidelity graphic simulation of a telerobot (called Phantom Robot) is used for preview and predictive displays for planning and for real-time control under several seconds communication time delay conditions. High fidelity graphic simulation is obtained by using appropriate calibration techniques
Protective Intestinal Effects of Pituitary Adenylate Cyclase Activating Polypeptide
Pituitary adenylate cyclase activating polypeptide (PACAP) is an
endogenous neuropeptide widely distributed throughout the body, including the
gastrointestinal tract. Several effects have been described in human and animal
intestines. Among others, PACAP infl uences secretion of intestinal glands, blood
fl ow, and smooth muscle contraction. PACAP is a well-known cytoprotective peptide
with strong anti-apoptotic, anti-infl ammatory, and antioxidant effects. The
present review gives an overview of the intestinal protective actions of this neuropeptide.
Exogenous PACAP treatment was protective in a rat model of small bowel
autotransplantation. Radioimmunoassay (RIA) analysis of the intestinal tissue showed that endogenous PACAP levels gradually decreased with longer-lasting
ischemic periods, prevented by PACAP addition. PACAP counteracted deleterious
effects of ischemia on oxidative stress markers and cytokines. Another series of
experiments investigated the role of endogenous PACAP in intestines in PACAP
knockout (KO) mice. Warm ischemia–reperfusion injury and cold preservation models
showed that the lack of PACAP caused a higher vulnerability against ischemic
periods. Changes were more severe in PACAP KO mice at all examined time points.
This fi nding was supported by increased levels of oxidative stress markers and
decreased expression of antioxidant molecules. PACAP was proven to be protective
not only in ischemic but also in infl ammatory bowel diseases. A recent study showed
that PACAP treatment prolonged survival of Toxoplasma gondii infected mice suffering
from acute ileitis and was able to reduce the ileal expression of proinfl ammatory
cytokines. We completed the present review with recent clinical results obtained
in patients suffering from infl ammatory bowel diseases. It was found that PACAP
levels were altered depending on the activity, type of the disease, and antibiotic
therapy, suggesting its probable role in infl ammatory events of the intestine
Lower Respiratory Tract Infection Induced by a Genetically Modified Picornavirus in Its Natural Murine Host
Infections with the picornavirus, human rhinovirus (HRV), are a major cause of wheezing illnesses and asthma exacerbations. In developing a murine model of picornaviral airway infection, we noted the absence of murine rhinoviruses and that mice are not natural hosts for HRV. The picornavirus, mengovirus, induces lethal systemic infections in its natural murine hosts, but small genetic differences can profoundly affect picornaviral tropism and virulence. We demonstrate that inhalation of a genetically attenuated mengovirus, vMC0, induces lower respiratory tract infections in mice. After intranasal vMC0 inoculation, lung viral titers increased, peaking at 24 h postinoculation with viral shedding persisting for 5 days, whereas HRV-A01a lung viral titers decreased and were undetectable 24 h after intranasal inoculation. Inhalation of vMC0, but not vehicle or UV-inactivated vMC0, induced an acute respiratory illness, with body weight loss and lower airway inflammation, characterized by increased numbers of airway neutrophils and lymphocytes and elevated pulmonary expression of neutrophil chemoattractant CXCR2 ligands (CXCL1, CXCL2, CXCL5) and interleukin-17A. Mice inoculated with vMC0, compared with those inoculated with vehicle or UV-inactivated vMC0, exhibited increased pulmonary expression of interferon (IFN-α, IFN-β, IFN-λ), viral RNA sensors [toll-like receptor (TLR)3, TLR7, nucleotide-binding oligomerization domain containing 2 (NOD2)], and chemokines associated with HRV infection in humans (CXCL10, CCL2). Inhalation of vMC0, but not vehicle or UV-inactivated vMC0, was accompanied by increased airway fluid myeloperoxidase levels, an indicator of neutrophil activation, increased MUC5B gene expression, and lung edema, a sign of infection-related lung injury. Consistent with experimental HRV inoculations of nonallergic, nonasthmatic human subjects, there were no effects on airway hyperresponsiveness after inhalation of vMC0 by healthy mice. This novel murine model of picornaviral airway infection and inflammation should be useful for defining mechanisms of HRV pathogenesis in humans
PACAP is an endogenous protective factor - insights from PACAP-deficient mice
Pituitary adenylate cyclase-activating polypeptide (PACAP) is a
widespread neuropeptide with a diverse array of biological
functions. Not surprisingly, the lack of endogenous PACAP
therefore results in a variety of abnormalities. One of the
important effects of PACAP is its neuroprotective and general
cytoprotective role. PACAP protects neurons and other tissues
against ischemic, toxic, and traumatic lesions. Data obtained
from PACAP-deficient mice provide evidence that endogenous
PACAP also has protective functions. Mice lacking PACAP are more
vulnerable to different in vitro and in vivo insults. The
present review summarizes data on the increased sensitivity of
PACAP-deficient mice against harmful stimuli. Mice lacking PACAP
respond with a higher degree of injury in cerebral ischemia,
autoimmune encephalomyelitis, and axonal lesion. Retinal
ischemic and excitotoxic injuries also produce increased cell
loss in PACAP-deficient mice. In peripheral organs, kidney cell
cultures from PACAP-deficient mice are more sensitive to
oxidative stress and in vitro hypoxia. In vivo, PACAP-deficient
mice have a negative histological outcome and altered cytokine
response in kidney and small intestine ischemia/reperfusion
injury. Large intestinal inflammation, toxic lesion of the
pancreas, and doxorubicin-induced cardiomyopathy are also more
severe with a lack of endogenous PACAP. Finally, an increased
inflammatory response has been described in subacute endotoxin-
induced airway inflammation and in an oxazolone-induced allergic
contact dermatitis model. In summary, lack of endogenous PACAP
leads to higher vulnerability in a number of injuries in the
nervous system and peripheral organs, supporting the hypothesis
that PACAP is part of the endogenous cytoprotective machinery