Kinematic models and human elbow flexion movements: Quantitative analysis

Summary The smoothness with which movements are customarily performed has led Hogan (1984) to formulate a model for trajectory planning by the central nervous system in which the goal is to maximize smoothness, one measure of which is the integrated mean squared magnitude of jerk (jerk cost). We tested the applicability of this minimum-jerk model to one-joint goal directed movements performed by human subjects at different speeds and amplitudes, by comparing kinematic parameters and the jerk cost predicted by the mathematical model with values calculated from experimental data. We also tested a higher order, minimum-snap kinematic model. Normal subjects performed elbow flexions of 5 to 50 degrees as rapidly and accurately as possible and also at slower speeds. The boundary conditions of both models were adjusted to account for the failure of subjects to produce movements which reached equilibrium precisely at the target (so that acceleration and velocity reached zero together). Typically, fast movements (< 300 ms duration) were fairly symmetric in that the durations and amplitudes of acceleration and deceleration were approximately equal; slower movements (> 300ms) were asymmetric with strong, brief acceleration peaks and broad, slow deceleration peaks. In fast movements, the calculated jerk cost was consistently higher than predicted by the minimum-jerk model; a good fit to all kinematic parameters was provided by the minimum-snap model (a seventh-order polynomial). Neither model consistently predicted the trajectories of slower movements. We conclude that muscle/limb dynamics can account for the success of the minimum-snap model with fast movements, and that there is no evidence of planning for maximal smoothness in slower movements.     

Effects of weak antagonist on fast elbow flexion movements in man

Summary By using a mathematical model and experiments involving electrical simulation of antagonistic muscles, we have formed the hypothesis (Wierzbicka et al. 1986) that in one-joint movements the antagonist muscle not only provides braking torque but also controls movement time. To get additional experimental support for this hypothesis, we studied elbow flexion movements performed by patients with spinal cord injury at the C 5–6 level who had relatively normal strength in their biceps muscle and little or no voluntary control of the triceps. Seven quadriplegic patients and six control subjects performed elbow flexion movements of 10°, 20°, and 30° as fast and accurately as possible. Despite the lack of antagonist, patients used the same pulse height strategy as control subjects to scale their responses with movement amplitude. However, patients' movement time was on average twice that of control subjects, and durations of both accelerative and decelerative phases of movement were increased. Movement speed and acceleration were reduced to 20–50% of the corresponding values of control subjects. Patients tended to overshoot the target to a larger extent than control subjects, particularly 10° targets, with nearly twice the error. We performed the same experiments using an external torque motor to assist the weak triceps. When a constant extensor torque of 2.5 or 5 Nm was provided by the motor, patients were able to move faster, and movement accuracy improved to within the normal range. These results provide direct evidence that the lack of an antagonist has an important effect on completion time and accuracy of fast goal-directed movements.     

The influence of the SARS-CoV-2 pandemic on oral and maxillofacial surgery: a nationwide survey among 54 hospitals and 240 private practices in Germany

Clinical Oral Investigations - The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) pandemic has created hitherto unknown challenges for healthcare systems and patient care. This study...     

Role of agonist and antagonist muscles in fast arm movements in man

Summary Fast goal-directed voluntary movements of the human upper extremity are known to be associated with three distinct bursts of EMG activity in antagonistic muscles. The role of each burst (AG1, ANT, AG2) in controlling motion is not fully understood, largely because overall limb response is a complex function of the entire sequence of bursts recorded during experimental trials. In order to investigate the role of each burst of muscle activity in controlling motion, we studied fast voluntary arm movements and also developed two simulation techniques, one employing a mathematical model of the limb and the other using electrical stimulation of human arm muscles. These techniques show that two important movement parameters (peak displacement, time to reach peak displacement) are non-linear functions of the magnitude of the antagonist input (torque and stimulation voltage, respectively, in our two simulations). In the fastest movements, the agonist muscle is primarily responsible for the distance moved, while the antagonist muscle provides an effective means of reducing movement time. The third component of the triphasic pattern moderates the antagonist braking forces and redirects the movement back to the target.     

Effects of muscle thixotropy on afferent activity in the hindlimb of the rat

The increase with time of the stiffness of resting muscle and its effect on afferent nerve activity arising within the muscle were investigated in the leg of the anaesthetized rat. Nerve activity was recorded from the branch of the tibial nerve innervating the gastrocnemius muscle. A sinusoidal torque from a motor coaxial with the ankle produced small (less than 0.25 deg) oscillations of the resting foot that were interrupted by several cycles of a much larger amplitude displacement. After the perturbation, the same small torque caused larger (greater than 0.40 deg) oscillations, demonstrating a reduction in the resting or short-range stiffness of muscles acting at the joint. Turning off the torque for 30 s allowed the stiffness to return to its enhanced level. Afferent nerve activity in response to the small torque was greater following the perturbation, reflecting the larger oscillations. We conclude that thixotropic stiffening of muscles at rest reduces postural displacements produced by small torques as well as the quantity of afferent signals converging on the central nervous system from these events.     

Effects of hypertrophy and allylamine-induced fibrosis on mechanical properties of isolated rat heart muscles with references to the pumping function of the intact heart in the same models

To examine the effects of hypertrophy and fibrosis on myocardial mechanics, we studied isolated left ventricular papillary muscles from 6-month-old male SHR and allylamine-fed rats. In SHR, the peak developed tension (DT) and the maximum rate of tension development (dT/dt) were higher compared to control male Wistar-Kyoto rats (WKY). With 15 min of hypoxia, the DT and the dT/dt declined similarly in both groups and the ratios of DT and dT/dt to their prehypoxic values after 15 min of hypoxia were not different in the two groups. From allylamine-fed rats, only 4 papillary muscles had more than 25% interstitial fibrosis by point-counting (AL-B group), but 9 muscles had no fibrotic involvement and their left ventricular hydroxyproline concentration was normal (AL-A group). The myocardial diameters, the passive stiffness constant and the duration of isometric contractions at Lmax were increased in AL-B group, but the resting tension, the DT at Lmax and the force-velocity relations did not differ from controls. The mechanical properties of the AL-A group muscles were not different from controls. However, when pumping function was examined in the intact heart from the AL-A group, the LVEDP was increased and the peak cardiac output normalized by body weight was decreased. Thus, hypertrophied muscle from SHR shows hyperfunction without an increase in susceptibility to hypoxic stress. Even if fibrosis progresses, hypertrophy can compensate for the reduction in contractile component up to a certain degree.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy of an implanted neuroprosthesis for restoring hand grasp in tetraplegia: a multicenter study

OBJECTIVE: To evaluate an implanted neuroprosthesis that allows tetraplegic users to control grasp and release in 1 hand. DESIGN: Multicenter cohort trial with at least 3 years of follow-up. Function for each participant was compared before and after implantation, and with and without the neuroprosthesis activated. SETTING: Tertiary spinal cord injury (SCI) care centers, 8 in the United States, 1 in the United Kingdom, and 1 in Australia. PARTICIPANTS: Fifty-one tetraplegic adults with C5 or C6 SCIs. INTERVENTION: An implanted neuroprosthetic system, in which electric stimulation of the grasping muscles of 1 arm are controlled by using contralateral shoulder movements, and concurrent tendon transfer surgery. Assessed participants' ability to grasp, move, and release standardized objects; degree of assistance required to perform activities of daily living (ADLs), device usage; and user satisfaction. MAIN OUTCOME MEASURES: Pinch force; grasp and release tests; ADL abilities test and ADL assessment test; and user satisfaction survey. RESULTS: Pinch force was significantly greater with the neuroprosthesis in all available 50 participants, and grasp-release abilities were improved in 49. All tested participants (49/49) were more independent in performing ADLs with the neuroprosthesis than they were without it. Home use of the device for regular function and exercise was reported by over 90% of the participants, and satisfaction with the neuroprosthesis was high. CONCLUSIONS: The grasping ability provided by the neuroprosthesis is substantial and lasting. The neuroprosthesis is safe, well accepted by users, and offers improved independence for a population without comparable alternatives.     

Controversies in radiotherapy for pediatric Hodgkin's lymphoma

Cure rates for pediatric Hodgkin's lymphoma remain among the highest in pediatric oncology. Research efforts are currently focused on minimizing treatment-related toxicity without compromising outcomes. For children with early stage/favorable Hodgkin's lymphoma, the standard treatment includes 2-4 cycles of combination chemotherapy, generally followed by low-dose involved-field radiotherapy. Children with advanced stage/unfavorable disease require more intense treatment than those with favorable disease. The standard treatment for advanced stage/unfavorable disease is 4–6 cycles of intense multiagent non-cross-resistant chemotherapy and involved-field radiotherapy. Response-adapted therapy is emerging as a promising strategy to attenuate therapy and thereby reduce toxicity in children with an excellent prognosis and intensify therapy in those children at higher risk of progression or relapse.     

Prevention of autoimmune diabetes with nonactivating anti-CD3 monoclonal antibody.

Autoreactive T cells mediate diabetes in animal models of insulin-dependent diabetes mellitus (IDDM) and are believed to cause the disease in humans. Therefore, immunotherapies directed against T cells are of particular interest for the treatment of IDDM. One candidate for such immunotherapy is anti-CD3 monoclonal antibodies (MoAbs), but clinical side effects are common with anti-CD3 treatment due to the ability of these MoAbs to activate T cells in vivo. However, F(ab')2 fragments of anti-CD3 are nonactivating and immunosuppressive. We evaluated the effects of whole anti-CD3 MoAb and F(ab')2 fragments in the setting of experimental autoimmune diabetes. Treatment with whole MoAb or F(ab')2 fragments significantly reduced the hyperglycemia induced with multiple low dosages of streptozocin (MDSDM; 232 +/- 23 mg/dl, P less than 0.01 and 235 +/- 16 mg/dl, P less than 0.01 vs. 325 +/- 25 mg/dl, respectively) in male CD1 mice. Both whole MoAb and F(ab')2 fragments suppressed the development of insulitis (P less than 0.001). Treatment with whole MoAb resulted in marked weight loss (10.4 +/- 1.5% of total body wt), and the mice appeared ill and listless, whereas, mice treated with F(ab')2 fragments gained weight (4.9 +/- 5.5% of total body wt) and appeared healthy. Treatment with whole MoAb caused activation of T cells in vivo as reflected by proliferation of freshly isolated spleen cells to recombinant interleukin-2. Depletion of T cells with whole MoAb was more pronounced than with F(ab')2 fragments, and T-cell receptor (TCR) reexpression on remaining cells occurred with F(ab')2 fragments within 48 h after F(ab')2 treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Complement C5a‐Induced Changes in Neutrophil Morphology During Inflammation

The complement and neutrophil defence systems, as major components of innate immunity, are activated during inflammation and infection. For neutrophil migration to the inflamed region, we hypothesized that the complement activation product C5a induces significant changes in cellular morphology before chemotaxis. Exposure of human neutrophils to C5a dose‐ and time‐dependently resulted in a rapid C5a receptor‐1 (C5aR1)‐dependent shape change, indicated by enhanced flow cytometric forward‐scatter area values. Similar changes were observed after incubation with zymosan‐activated serum and in blood neutrophils during murine sepsis, but not in mice lacking the C5aR1. In human neutrophils, Amnis high‐resolution digital imaging revealed a C5a‐induced decrease in circularity and increase in the cellular length/width ratio. Biomechanically, microfluidic optical stretching experiments indicated significantly increased neutrophil deformability early after C5a stimulation. The C5a‐induced shape changes were inhibited by pharmacological blockade of either the ‐exchanger or the Cl⁻‐channel. Furthermore, actin polymerization assays revealed that C5a exposure resulted in a significant polarization of the neutrophils. The functional polarization process triggered by ATP–P2X/Y‐purinoceptor interaction was also involved in the C5a‐induced shape changes, because pretreatment with suramin blocked not only the shape changes but also the subsequent C5a‐dependent chemotactic activity. In conclusion, the data suggest that the anaphylatoxin C5a regulates basic neutrophil cell processes by increasing the membrane elasticity and cell size as a consequence of actin‐cytoskeleton polymerization and reorganization, transforming the neutrophil into a migratory cell able to invade the inflammatory site and subsequently clear pathogens and molecular debris.