From milanos@imi.bg.ac.yu  Mon Jan  4 16:38:38 1999
Return-Path: <milanos@imi.bg.ac.yu>
Received: from magelan.vet.bg.ac.yu ([147.91.250.6] (may be forged))
	by Mala.vet.bg.ac.yu (8.8.6/8.8.5) with SMTP id QAA30464
	for <tony@mala.vet.bg.ac.yu>; Mon, 4 Jan 1999 16:38:37 +0100
Received: from imi1 (unverified [147.91.250.220]) by magelan.vet.bg.ac.yu
 (EMWAC SMTPRS 0.83) with SMTP id <B0000008731@magelan.vet.bg.ac.yu>;
 Mon, 04 Jan 1999 16:42:39 +0100
Message-Id: <3.0.1.32.19990104163806.006df408@imi.bg.ac.yu>
X-Sender: milanos@imi.bg.ac.yu
X-Mailer: Windows Eudora Light Version 3.0.1 (32)
Date: Mon, 04 Jan 1999 16:38:06 +0100
To: tony@mala.vet.bg.ac.yu
From: Sladjan Milanovic <milanos@imi.bg.ac.yu>
Subject: formati
Mime-Version: 1.0
Content-Type: multipart/mixed; boundary="=====================_915460686==_"
Status: RO
X-Status: 

--=====================_915460686==_
Content-Type: text/plain; charset="us-ascii"

Cao Tony,


1. Medlars (Bookend/Getaref)

2. RIS (Reference Manager/ProCite)

3. EndNote (Refer/BIBIX)

ka o attach ti idu file-ovi koji odgovaraju rednim brojevima ovih formata




a za ostalo pogledaj ovo. Mislim da sam ti vec poslao link:

http://crysta.physik.hu-berlin.de/~boeck/Sixpack/

ovo je software  za Reference

pozdrav,
S.
--=====================_915460686==_
Content-Type: text/plain; charset="iso-8859-1"
Content-Transfer-Encoding: quoted-printable
Content-Disposition: attachment; filename="1.txt"

UI  - 98290367
AU  - Jaric, S.
AU  - Gottlieb, G.L.
AU  - Latash, M.L.
AU  - Corcos, D.M.
TI  - Changes in the symmetry of rapid movements. Effects of velocity and=
 viscosity.
LA  - Eng
MH  - Adult
MH  - Comparative Study
MH  - Elbow Joint
MH  - Electromyography
MH  - Human
MH  - Linear Models
MH  - Male
MH  - Movement
MH  - Reaction Time
MH  - Support, Non-U.S. Gov't
MH  - Support, U.S. Gov't, Non-P.H.S.
MH  - Support, U.S. Gov't, P.H.S.
MH  - Viscosity
MH  - Weight-Bearing
PT  - CLINICAL TRIAL
PT  - JOURNAL ARTICLE
PT  - RANDOMIZED CONTROLLED TRIAL
DA  - 980827
DP  - 1998
IS  - 0014-4819
TA  - Exp Brain Res
PG  - 52-60
DA  - M
CY  - GERMANY
VI  - 120
JC  - EP2
EM  - 9810
AD  - Faculty for Physical Culture, University of Belgrade, Yugoslavia.
AB  - Five subjects made rapid, discrete elbow flexion movements over=
 different distances, against different inertial loads, as well as under=
 distance and load combinations that kept movement time constant. The=
 results demonstrated that an increase in peak movement velocity was=
 associated with an increase in the temporal symmetry ratio of the movement=
 (acceleration time divided by deceleration time), as well as with an=
 increase in both agonist electromyographic (EMG) burst duration and=
 antagonist EMG latency. Since an increase in peak movement velocity is=
 associated with faster agonist muscle shortening, as well as with faster=
 stretching of the antagonist muscle, we hypothesize that the=
 velocity-related changes in movement symmetry can be viewed as, at least=
 partially, a consequence of muscle viscosity. Viscosity increasingly=
 resists the shortening agonist and assists the lengthening antagonist when=
 movement velocity increases. Therefore, the agonist muscles require more=
 time to produce the required impulse, while the antagonist muscle can brake=
 the movement in a shorter period of time. In order to test the hypothesis=
 that viscosity is responsible for the velocity-associated changes in the=
 symmetry ratio, we performed a second experiment with distance and load=
 combinations identical to those of the first experiment, but with different=
 external viscous loads, which resisted the slower and assisted the faster=
 movements. The results demonstrated that the movements became more=
 symmetrical in the presence of the viscous load. There were also changes in=
 agonist duration and antagonist latency. We conclude that changes in the=
 symmetry associated with changes in movement velocity may be due to the=
 effects of either muscle viscosity or changes in how muscles are activated=
 to account for differences in viscous force.
SO  - Exp Brain Res 1998;120:52-60

UI  - 98165876
AU  - Gribble, P.L.
AU  - Ostry, D.J.
AU  - Sanguineti, V.
AU  - Laboissiere, R.
TI  - Are complex control signals required for human arm movement?
LA  - Eng
MH  - Arm
MH  - Hand
MH  - Human
MH  - Joints
MH  - Mathematics
MH  - Models, Biological
MH  - Motor Activity
MH  - Movement
MH  - Muscle Contraction
MH  - Muscle, Skeletal
MH  - Reaction Time
MH  - Reflex
MH  - Support, Non-U.S. Gov't
MH  - Support, U.S. Gov't, P.H.S.
PT  - JOURNAL ARTICLE
DA  - 980424
DP  - 1998
IS  - 0022-3077
TA  - J Neurophysiol
PG  - 1409-24
DA  - M
CY  - UNITED STATES
VI  - 79
JC  - JC7
EM  - 9807
AD  - Department of Psychology, McGill University, Montreal, Quebec H3A 1B1,=
 Canada.
AB  - It has been proposed that the control signals underlying voluntary=
 human arm movement have a "complex" nonmonotonic time-varying form, and a=
 number of empirical findings have been offered in support of this idea. In=
 this paper, we address three such findings using a model of two-joint arm=
 motion based on the lambda version of the equilibrium-point hypothesis. The=
 model includes six one- and two-joint muscles, reflexes, modeled control=
 signals, muscle properties, and limb dynamics. First, we address the claim=
 that "complex" equilibrium trajectories are required to account for=
 nonmonotonic joint impedance patterns observed during multijoint movement.=
 Using constant-rate shifts in the neurally specified equilibrium of the=
 limb and constant cocontraction commands, we obtain patterns of predicted=
 joint stiffness during simulated multijoint movements that match the=
 nonmonotonic patterns reported empirically. We then use the algorithm=
 proposed by Gomi and Kawato to compute a hypothetical equilibrium=
 trajectory from simulated stiffness, viscosity, and limb kinematics. Like=
 that reported by Gomi and Kawato, the resulting trajectory was=
 nonmonotonic, first leading then lagging the position of the limb. Second,=
 we address the claim that high levels of stiffness are required to generate=
 rapid single-joint movements when simple equilibrium shifts are used. We=
 compare empirical measurements of stiffness during rapid single-joint=
 movements with the predicted stiffness of movements generated using=
 constant-rate equilibrium shifts and constant cocontraction commands.=
 Single-joint movements are simulated at a number of speeds, and the=
 procedure used by Bennett to estimate stiffness is followed. We show that=
 when the magnitude of the cocontraction command is scaled in proportion to=
 movement speed, simulated joint stiffness varies with movement speed in a=
 manner comparable with that reported by Bennett. Third, we address the=
 related claim that nonmonotonic equilibrium shifts are required to generate=
 rapid single-joint movements. Using constant-rate equilibrium shifts and=
 constant cocontraction commands, rapid single-joint movements are simulated=
 in the presence of external torques. We use the procedure reported by=
 Latash and Gottlieb to compute hypothetical equilibrium trajectories from=
 simulated torque and angle measurements during movement. As in Latash and=
 Gottlieb, a nonmonotonic function is obtained even though the control=
 signals used in the simulations are constant-rate changes in the=
 equilibrium position of the limb. Differences between the "simple"=
 equilibrium trajectory proposed in the present paper and those that are=
 derived from the procedures used by Gomi and Kawato and Latash and Gottlieb=
 arise from their use of simplified models of force generation.
SO  - J Neurophysiol 1998;79:1409-24

UI  - 94275656
AU  - Bennett, D.J.
TI  - Stretch reflex responses in the human elbow joint during a voluntary=
 movement.
LA  - Eng
MH  - Adult
MH  - Elasticity
MH  - Elbow Joint
MH  - Electromyography
MH  - Female
MH  - Human
MH  - Male
MH  - Movement
MH  - Muscles
MH  - Reflex, Stretch
MH  - Support, Non-U.S. Gov't
MH  - Viscosity
PT  - JOURNAL ARTICLE
DA  - 940719
DP  - 1994
IS  - 0022-3751
TA  - J Physiol (Lond)
PG  - 339-51
DA  - M
CY  - ENGLAND
VI  - 474
JC  - JQV
EM  - 9409
AD  - Department of Brain and Cognitive Sciences, Massachusetts Institute of=
 Technology, Cambridge 01239.
AB  - 1. The responsiveness of the stretch reflex is modulated during human=
 voluntary limb movements. The influence of this modulation on the limb=
 mechanical properties (stiffness) was investigated. 2. Subjects were taught=
 to replicate accurately a rapid (4.0 rad s-1) targeted elbow flexion=
 movement of 1 rad. From the onset of 12% of the trials a sinusoidal=
 position disturbance (0.05 rad) was superimposed on the normal (trained)=
 movement trajectory. The net joint torque (muscle torque) resisting these=
 stretches was computed from measurements of applied torque, acceleration=
 and limb inertia. Electromyographic (EMG) responses in the triceps brachii=
 (TB), brachialis (Br) and biceps brachii (BB) were monitored. 3. The EMG=
 responses to sinusoidal stretches applied early in the movement were less=
 than those responses to perturbations applied when the arm neared the=
 target (especially in the antagonist muscle TB). These EMG responses caused=
 fluctuations in the resistance to the perturbation (stiffness), as=
 described below. 4. When the perturbation frequency was low (< 4 Hz) the=
 resistance of the elbow muscles to the stretch increased as the arm=
 approached the target (48% increase). In contrast, when the stretch=
 frequency was 7 Hz the resistance decreased by 63%. This decrease can be=
 explained by the increased reflex response, since at 7 Hz the reflex=
 response is probably timed so that it assists, rather than resists, the=
 stretching as a result of loop delays. This reflex timing was confirmed by=
 observing that, after abruptly stopping the sinusoidal stretch, the reflex=
 response persisted for 100 ms and was indeed in a direction that would have=
 reduced the resistance, had the perturbation continued. 5. The time course=
 of the net muscle stiffness was estimated for frequencies ranging from 4 to=
 8 Hz and for each 40 ms interval a Nyquist plot was constructed, forming a=
 C-shaped curve as frequency was varied. The size of this curve gave a=
 measure of the stiffness resulting from reflex activity. When the arm=
 neared the target this reflexive stiffness reached a maximum, and was=
 probably comparable in size to the intrinsic (non-reflexive) muscle=
 stiffness. Also, in four of the five subjects the viscous component of=
 stiffness at 7 Hz dropped significantly below zero when the arm neared the=
 target, again indicating that at this frequency the reflex was large and=
 acted inappropriately.(ABSTRACT TRUNCATED AT 400 WORDS)
SO  - J Physiol (Lond) 1994;474:339-51

UI  - 86196249
AU  - Dingus, J.
AU  - Hwo, S.
AU  - Bryan, J.
TI  - Identification by monoclonal antibodies and characterization of human=
 platelet caldesmon.
LA  - Eng
MH  - Animal
MH  - Antibodies, Monoclonal
MH  - Blood Platelets
MH  - Calmodulin
MH  - Calmodulin-Binding Proteins
MH  - Carrier Proteins
MH  - Chickens
MH  - Fluorescent Antibody Technique
MH  - Gels
MH  - Gizzard
MH  - Human
MH  - Microfilament Proteins
MH  - Molecular Weight
RN  - 0 (brevin)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Calmodulin)
RN  - 0 (Calmodulin-Binding Proteins)
RN  - 0 (Carrier Proteins)
RN  - 0 (Gels)
RN  - 0 (Microfilament Proteins)
PT  - JOURNAL=20ARTICLE
DA  - 860612
DP  - 1986
IS  - 0021-9525
TA  - J Cell Biol
PG  - 1748-57
DA  - M X
CY  - UNITED STATES
VI  - 102
JC  - HMV
EM  - 8608
CU  - 92
AB  - Actin-based gels were prepared from clarified high-salt extracts of=
 human platelets by dialysis against physiological salt buffers. The gel was=
 partially solubilized with 0.3 M KCl. Mice were immunized with the 0.3 M=
 KCl extract of the actin gel, and hybridomas were produced by fusion of=
 spleen cells with myeloma cells. Three hybridomas were generated that=
 secrete antibodies against an 80-kD protein. These monoclonal antibodies=
 stained stress fibers in cultured cells and cross-reacted with proteins in=
 several tissue types, including smooth muscle. The cross-reacting protein=
 in chicken gizzard smooth muscle had an apparent molecular weight of=
 140,000 and was demonstrated to be caldesmon, a calmodulin and=
 actin-binding protein (Sobue, K., Y. Muramoto, M. Fujita, and S. Kakiuchi,=
 Proc. Natl. Acad. Sci. USA, 78:5652-5655). No proteins of molecular weight=
 greater than 80 kD were detectable in platelets by immunoblotting using the=
 monoclonal antibodies. The 80-kD protein is heat stable and was purified=
 using modifications of the procedure reported by Bretscher for the rapid=
 purification of smooth muscle caldesmon (Bretscher, A., 1985, J. Biol.=
 Chem., 259:12873-12880). The 80-kD protein bound to calmodulin-Sepharose in=
 a Ca++-dependent manner and sedimented with actin filaments, but did not=
 greatly increase the viscosity of F-actin solutions. The actin-binding=
 activity was inhibited by calmodulin in the presence of calcium. Except for=
 the molecular weight difference, the 80-kD platelet protein appears=
 functionally similar to 140-kD smooth muscle caldesmon. We propose that the=
 80-kD protein is platelet caldesmon.
SO  - J Cell Biol 1986;102:1748-57

UI  - 86088110
AU  - Ravussin, P.
AU  - Archer, D.P.
AU  - Tyler, J.L.
AU  - Meyer, E.
AU  - Abou-Madi, M.
AU  - Diksic, M.
AU  - Yamamoto, L.
AU  - Trop, D.
TI  - Effects of rapid mannitol infusion on cerebral blood volume. A=
 positron emission tomographic study in dogs and man.
LA  - Eng
MH  - Adult
MH  - Animal
MH  - Blood Pressure
MH  - Blood Volume
MH  - Brain
MH  - Dogs
MH  - Heart Rate
MH  - Human
MH  - Intracranial Pressure
MH  - Male
MH  - Mannitol
MH  - Middle Age
MH  - Potassium
MH  - Support, Non-U.S. Gov't
MH  - Tomography, Emission-Computed
RN  - 69-65-8 (Mannitol)
RN  - 7440-09-7 (Potassium)
PT  - JOURNAL ARTICLE
DA  - 860127
DP  - 1986
IS  - 0022-3085
TA  - J Neurosurg
PG  - 104-13
DA  - A M X
CY  - UNITED STATES
VI  - 64
JC  - JD3
EM  - 8604
CU  - 91
AB  - Positron emission tomography was used to study the effect of a rapid=
 infusion of mannitol on cerebral blood volume (CBV) in five dogs and in=
 three human subjects. The ability of mannitol to reduce intracranial=
 pressure (ICP) has always been attributed to its osmotic dehydrating=
 effect. The effects of mannitol infusion include increased osmolality,=
 total blood volume, central venous pressure (CVP), and cerebral blood flow,=
 and decreased hematocrit, hemoglobin concentration, serum sodium level, and=
 viscosity. Mannitol's ability to dilate the cerebral vasculature, either=
 directly or indirectly, and thus to transiently increase ICP, is a subject=
 of controversy. By in vivo labeling of red cells with carbon-11, the=
 authors were able to demonstrate an early increase in CBV in dogs of 20%,=
 27%, and 23% (mean increase, p less than 0.05) at 1, 2, and 3 minutes,=
 respectively, after an infusion of 20% mannitol (2 gm/kg over a 3-minute=
 period). The animals' muscle blood volume increased by 27% (mean increase,=
 p less than 0.05) 2 minutes after infusion. In the human subjects, lower=
 doses and a longer duration of infusion (1 gm/kg over 4 minutes) resulted=
 in an increase in CBV of 8%, 14% (p less than 0.05), and 10% at 1, 2, and 3=
 minutes, respectively, after infusion. In dogs, ICP increased by 4 mm Hg=
 (mean increase, p less than 0.05) 1 minute after the infusion, before=
 decreasing sharply. The ICP was not measured in the human subjects.=
 Hematocrit, hemoglobin, sodium, potassium, osmolality, heart rate, mean=
 arterial pressure (MAP), and CVP were measured serially. Results of these=
 measurements, as well as the significant decrease in MAP that occurred=
 after mannitol infusion, are discussed. This study demonstrated that rapid=
 mannitol infusion increases CBV and ICP. The increase in muscle blood=
 volume, in the presence of a decreased MAP and an adequate CVP, suggests=
 that mannitol may have caused vasodilation in these experiments.
SO  - J Neurosurg 1986;64:104-13

--=====================_915460686==_
Content-Type: text/plain; charset="iso-8859-1"
Content-Transfer-Encoding: quoted-printable
Content-Disposition: attachment; filename="2.txt"

1
TY  - JOUR
N1  - 98290367
AU  - Jaric, S.
AU  - Gottlieb, G.L.
AU  - Latash, M.L.
AU  - Corcos, D.M.
TI  - Changes in the symmetry of rapid movements. Effects of velocity and=
 viscosity.
JO  - Exp Brain Res
VL  - 120
IS  - 1
SP  - 52
EP  - 60
PY  - 1998/// May
AD  - Faculty for Physical Culture, University of Belgrade, Yugoslavia.
AB  - Five subjects made rapid, discrete elbow flexion movements over=
 different distances, against different inertial loads, as well as under=
 distance and load combinations that kept movement time constant. The=
 results demonstrated that an increase in peak movement velocity was=
 associated with an increase in the temporal symmetry ratio of the movement=
 (acceleration time divided by deceleration time), as well as with an=
 increase in both agonist electromyographic (EMG) burst duration and=
 antagonist EMG latency. Since an increase in peak movement velocity is=
 associated with faster agonist muscle shortening, as well as with faster=
 stretching of the antagonist muscle, we hypothesize that the=
 velocity-related changes in movement symmetry can be viewed as, at least=
 partially, a consequence of muscle viscosity. Viscosity increasingly=
 resists the shortening agonist and assists the lengthening antagonist when=
 movement velocity increases. Therefore, the agonist muscles require more=
 time to produce the required impulse, while the antagonist muscle can brake=
 the movement in a shorter period of time. In order to test the hypothesis=
 that viscosity is responsible for the velocity-associated changes in the=
 symmetry ratio, we performed a second experiment with distance and load=
 combinations identical to those of the first experiment, but with different=
 external viscous loads, which resisted the slower and assisted the faster=
 movements. The results demonstrated that the movements became more=
 symmetrical in the presence of the viscous load. There were also changes in=
 agonist duration and antagonist latency. We conclude that changes in the=
 symmetry associated with changes in movement velocity may be due to the=
 effects of either muscle viscosity or changes in how muscles are activated=
 to account for differences in viscous force.
AB  - Type: CLINICAL TRIAL
AB  - Type: JOURNAL ARTICLE
AB  - Type: RANDOMIZED CONTROLLED TRIAL
SN  - 0014-4819
AB  - Language: Eng
KW  - Adult
KW  - Comparative Study
KW  - Elbow Joint
KW  - Electromyography
KW  - Human
KW  - Linear Models
KW  - Male
KW  - Movement
KW  - Reaction Time
KW  - Support, Non-U.S. Gov't
KW  - Support, U.S. Gov't, Non-P.H.S.
KW  - Support, U.S. Gov't, P.H.S.
KW  - Viscosity
KW  - Weight-Bearing
UR  - http://biomednet.com/db/medline/98290367
ER  -=20

2
TY  - JOUR
N1  - 98165876
AU  - Gribble, P.L.
AU  - Ostry, D.J.
AU  - Sanguineti, V.
AU  - Laboissiere, R.
TI  - Are complex control signals required for human arm movement?
JO  - J Neurophysiol
VL  - 79
IS  - 3
SP  - 1409
EP  - 1424
PY  - 1998/// Mar
AD  - Department of Psychology, McGill University, Montreal, Quebec H3A 1B1,=
 Canada.
AB  - It has been proposed that the control signals underlying voluntary=
 human arm movement have a "complex" nonmonotonic time-varying form, and a=
 number of empirical findings have been offered in support of this idea. In=
 this paper, we address three such findings using a model of two-joint arm=
 motion based on the lambda version of the equilibrium-point hypothesis. The=
 model includes six one- and two-joint muscles, reflexes, modeled control=
 signals, muscle properties, and limb dynamics. First, we address the claim=
 that "complex" equilibrium trajectories are required to account for=
 nonmonotonic joint impedance patterns observed during multijoint movement.=
 Using constant-rate shifts in the neurally specified equilibrium of the=
 limb and constant cocontraction commands, we obtain patterns of predicted=
 joint stiffness during simulated multijoint movements that match the=
 nonmonotonic patterns reported empirically. We then use the algorithm=
 proposed by Gomi and Kawato to compute a hypothetical equilibrium=
 trajectory from simulated stiffness, viscosity, and limb kinematics. Like=
 that reported by Gomi and Kawato, the resulting trajectory was=
 nonmonotonic, first leading then lagging the position of the limb. Second,=
 we address the claim that high levels of stiffness are required to generate=
 rapid single-joint movements when simple equilibrium shifts are used. We=
 compare empirical measurements of stiffness during rapid single-joint=
 movements with the predicted stiffness of movements generated using=
 constant-rate equilibrium shifts and constant cocontraction commands.=
 Single-joint movements are simulated at a number of speeds, and the=
 procedure used by Bennett to estimate stiffness is followed. We show that=
 when the magnitude of the cocontraction command is scaled in proportion to=
 movement speed, simulated joint stiffness varies with movement speed in a=
 manner comparable with that reported by Bennett. Third, we address the=
 related claim that nonmonotonic equilibrium shifts are required to generate=
 rapid single-joint movements. Using constant-rate equilibrium shifts and=
 constant cocontraction commands, rapid single-joint movements are simulated=
 in the presence of external torques. We use the procedure reported by=
 Latash and Gottlieb to compute hypothetical equilibrium trajectories from=
 simulated torque and angle measurements during movement. As in Latash and=
 Gottlieb, a nonmonotonic function is obtained even though the control=
 signals used in the simulations are constant-rate changes in the=
 equilibrium position of the limb. Differences between the "simple"=
 equilibrium trajectory proposed in the present paper and those that are=
 derived from the procedures used by Gomi and Kawato and Latash and Gottlieb=
 arise from their use of simplified models of force generation.
AB  - Type: JOURNAL ARTICLE
SN  - 0022-3077
AB  - Language: Eng
KW  - Arm
KW  - Hand
KW  - Human
KW  - Joints
KW  - Mathematics
KW  - Models, Biological
KW  - Motor Activity
KW  - Movement
KW  - Muscle Contraction
KW  - Muscle, Skeletal
KW  - Reaction Time
KW  - Reflex
KW  - Support, Non-U.S. Gov't
KW  - Support, U.S. Gov't, P.H.S.
UR  - http://biomednet.com/db/medline/98165876
ER  -=20

3
TY  - JOUR
N1  - 94275656
AU  - Bennett, D.J.
TI  - Stretch reflex responses in the human elbow joint during a voluntary=
 movement.
JO  - J Physiol (Lond)
VL  - 474
IS  - 2
SP  - 339
EP  - 351
PY  - 1994/// Jan 15
AD  - Department of Brain and Cognitive Sciences, Massachusetts Institute of=
 Technology, Cambridge 01239.
AB  - 1. The responsiveness of the stretch reflex is modulated during human=
 voluntary limb movements. The influence of this modulation on the limb=
 mechanical properties (stiffness) was investigated. 2. Subjects were taught=
 to replicate accurately a rapid (4.0 rad s-1) targeted elbow flexion=
 movement of 1 rad. From the onset of 12% of the trials a sinusoidal=
 position disturbance (0.05 rad) was superimposed on the normal (trained)=
 movement trajectory. The net joint torque (muscle torque) resisting these=
 stretches was computed from measurements of applied torque, acceleration=
 and limb inertia. Electromyographic (EMG) responses in the triceps brachii=
 (TB), brachialis (Br) and biceps brachii (BB) were monitored. 3. The EMG=
 responses to sinusoidal stretches applied early in the movement were less=
 than those responses to perturbations applied when the arm neared the=
 target (especially in the antagonist muscle TB). These EMG responses caused=
 fluctuations in the resistance to the perturbation (stiffness), as=
 described below. 4. When the perturbation frequency was low (< 4 Hz) the=
 resistance of the elbow muscles to the stretch increased as the arm=
 approached the target (48% increase). In contrast, when the stretch=
 frequency was 7 Hz the resistance decreased by 63%. This decrease can be=
 explained by the increased reflex response, since at 7 Hz the reflex=
 response is probably timed so that it assists, rather than resists, the=
 stretching as a result of loop delays. This reflex timing was confirmed by=
 observing that, after abruptly stopping the sinusoidal stretch, the reflex=
 response persisted for 100 ms and was indeed in a direction that would have=
 reduced the resistance, had the perturbation continued. 5. The time course=
 of the net muscle stiffness was estimated for frequencies ranging from 4 to=
 8 Hz and for each 40 ms interval a Nyquist plot was constructed, forming a=
 C-shaped curve as frequency was varied. The size of this curve gave a=
 measure of the stiffness resulting from reflex activity. When the arm=
 neared the target this reflexive stiffness reached a maximum, and was=
 probably comparable in size to the intrinsic (non-reflexive) muscle=
 stiffness. Also, in four of the five subjects the viscous component of=
 stiffness at 7 Hz dropped significantly below zero when the arm neared the=
 target, again indicating that at this frequency the reflex was large and=
 acted inappropriately.(ABSTRACT TRUNCATED AT 400 WORDS)
AB  - Type: JOURNAL ARTICLE
SN  - 0022-3751
AB  - Language: Eng
KW  - Adult
KW  - Elasticity
KW  - Elbow Joint
KW  - Electromyography
KW  - Female
KW  - Human
KW  - Male
KW  - Movement
KW  - Muscles
KW  - Reflex, Stretch
KW  - Support, Non-U.S. Gov't
KW  - Viscosity
UR  - http://biomednet.com/db/medline/94275656
ER  -=20

4
TY  - JOUR
N1  - 86196249
AU  - Dingus, J.
AU  - Hwo, S.
AU  - Bryan, J.
TI  - Identification by monoclonal antibodies and characterization of human=
 platelet caldesmon.
JO  - J Cell Biol
VL  - 102
IS  - 5
SP  - 1748
EP  - 1757
PY  - 1986/// May
AB  - Actin-based gels were prepared from clarified high-salt extracts of=
 human platelets by dialysis against physiological salt buffers. The gel was=
 partially solubilized with 0.3 M KCl. Mice were immunized with the 0.3 M=
 KCl extract of the actin gel, and hybridomas were produced by fusion of=
 spleen cells with myeloma cells. Three hybridomas were generated that secre=
te antibodies against an 80-kD protein. These monoclonal antibodies stained=
 stress fibers in cultured cells and cross-reacted with proteins in several=
 tissue types, including smooth muscle. The cross-reacting protein in=
 chicken gizzard smooth muscle had an apparent molecular weight of 140,000=
 and was demonstrated to be caldesmon, a calmodulin and actin-binding=
 protein (Sobue, K., Y. Muramoto, M. Fujita, and S. Kakiuchi, Proc. Natl.=
 Acad. Sci. USA, 78:5652-5655). No proteins of molecular weight greater than=
 80 kD were detectable in platelets by immunoblotting using the monoclonal=
 antibodies. The 80-kD protein is heat stable and was purified using=
 modifications of the procedure reported by Bretscher for the rapid=
 purification of smooth muscle caldesmon (Bretscher, A., 1985, J. Biol.=
 Chem., 259:12873-12880). The 80-kD protein bound to calmodulin-Sepharose in=
 a Ca++-dependent manner and sedimented with actin filaments, but did not=
 greatly increase the viscosity of F-actin solutions. The actin-binding=
 activity was inhibited by calmodulin in the presence of calcium. Except for=
 the molecular weight difference, the 80-kD platelet protein appears=
 functionally similar to 140-kD smooth muscle caldesmon. We propose that the=
 80-kD protein is platelet caldesmon.
AB  - Type: JOURNAL ARTICLE
SN  - 0021-9525
AB  - Language: Eng
KW  - Animal
KW  - Antibodies, Monoclonal
KW  - Blood Platelets
KW  - Calmodulin
KW  - Calmodulin-Binding Proteins
KW  - Carrier Proteins
KW  - Chickens
KW  - Fluorescent Antibody Technique
KW  - Gels
KW  - Gizzard
KW  - Human
KW  - Microfilament Proteins
KW  - Molecular Weight
UR  - http://biomednet.com/db/medline/86196249
ER  -=20

5
TY  - JOUR
N1  - 86088110
AU  - Ravussin, P.
AU  - Archer, D.P.
AU  - Tyler, J.L.
AU  - Meyer, E.
AU  - Abou-Madi, M.
AU  - Diksic, M.
AU  - Yamamoto, L.
AU  - Trop, D.
TI  - Effects of rapid mannitol infusion on cerebral blood volume. A=
 positron emission tomographic study in dogs and man.
JO  - J Neurosurg
VL  - 64
IS  - 1
SP  - 104
EP  - 113
PY  - 1986/// Jan
AB  - Positron emission tomography was used to study the effect of a rapid=
 infusion of mannitol on cerebral blood volume (CBV) in five dogs and in=
 three human subjects. The ability of mannitol to reduce intracranial=
 pressure (ICP) has always been attributed to its osmotic dehydrating=
 effect. The effects of mannitol infusion include increased osmolality,=
 total blood volume, central venous pressure (CVP), and cerebral blood flow,=
 and decreased hematocrit, hemoglobin concentration, serum sodium level, and=
 viscosity. Mannitol's ability to dilate the cerebral vasculature, either=
 directly or indirectly, and thus to transiently increase ICP, is a subject=
 of controversy. By in vivo labeling of red cells with carbon-11, the=
 authors were able to demonstrate an early increase in CBV in dogs of 20%,=
 27%, and 23% (mean increase, p less than 0.05) at 1, 2, and 3 minutes,=
 respectively, after an infusion of 20% mannitol (2 gm/kg over a 3-minute=
 period). The animals' muscle blood volume increased by 27% (mean increase,=
 p less than 0.05) 2 minutes after infusion. In the human subjects, lower=
 doses and a longer duration of infusion (1 gm/kg over 4 minutes) resulted=
 in an increase in CBV of 8%, 14% (p less than 0.05), and 10% at 1, 2, and 3=
 minutes, respectively, after infusion. In dogs, ICP increased by 4 mm Hg=
 (mean increase, p less than 0.05) 1 minute after the infusion, before=
 decreasing sharply. The ICP was not measured in the human subjects.=
 Hematocrit, hemoglobin, sodium, potassium, osmolality, heart rate, mean=
 arterial pressure (MAP), and CVP were measured serially. Results of these=
 measurements, as well as the significant decrease in MAP that occurred=
 after mannitol infusion, are discussed. This study demonstrated that rapid=
 mannitol infusion increases CBV and ICP. The increase in muscle blood=
 volume, in the presence of a decreased MAP and an adequate CVP, suggests=
 that mannitol may have caused vasodilation in these experiments.
AB  - Type: JOURNAL ARTICLE
SN  - 0022-3085
AB  - Language: Eng
KW  - Adult
KW  - Animal
KW  - Blood Pressure
KW  - Blood Volume
KW  - Brain
KW  - Dogs
KW  - Heart Rate
KW  - Human
KW  - Intracranial Pressure
KW  - Male
KW  - Mannitol
KW  - Middle Age
KW  - Potassium
KW  - Support, Non-U.S. Gov't
KW  - Tomography, Emission-Computed
UR  - http://biomednet.com/db/medline/86088110
ER  -=20

--=====================_915460686==_
Content-Type: text/plain; charset="iso-8859-1"
Content-Transfer-Encoding: quoted-printable
Content-Disposition: attachment; filename="3.txt"

%0 Journal Article
%1 98290367
%A Jaric, S.
%A Gottlieb, G.L.
%A Latash, M.L.
%A Corcos, D.M.
%T Changes in the symmetry of rapid movements. Effects of velocity and=
 viscosity
%J Exp Brain Res
%V 120
%N 1
%P 52-60
%D 1998
%O Faculty for Physical Culture, University of Belgrade, Yugoslavia.
%X Five subjects made rapid, discrete elbow flexion movements over different=
 distances, against different inertial loads, as well as under distance and=
 load combinations that kept movement time constant. The results=
 demonstrated that an increase in peak movement velocity was associated with=
 an increase in the temporal symmetry ratio of the movement (acceleration=
 time divided by deceleration time), as well as with an increase in both=
 agonist electromyographic (EMG) burst duration and antagonist EMG latency.=
 Since an increase in peak movement velocity is associated with faster=
 agonist muscle shortening, as well as with faster stretching of the=
 antagonist muscle, we hypothesize that the velocity-related changes in=
 movement symmetry can be viewed as, at least partially, a consequence of=
 muscle viscosity. Viscosity increasingly resists the shortening agonist and=
 assists the lengthening antagonist when movement velocity increases.=
 Therefore, the agonist muscles require more time to produce the required=
 impulse, while the antagonist muscle can brake the movement in a shorter=
 period of time. In order to test the hypothesis that viscosity is=
 responsible for the velocity-associated changes in the symmetry ratio, we=
 performed a second experiment with distance and load combinations identical=
 to those of the first experiment, but with different external viscous=
 loads, which resisted the slower and assisted the faster movements. The=
 results demonstrated that the movements became more symmetrical in the=
 presence of the viscous load. There were also changes in agonist duration=
 and antagonist latency. We conclude that changes in the symmetry associated=
 with changes in movement velocity may be due to the effects of either=
 muscle viscosity or changes in how muscles are activated to account for=
 differences in viscous force.
%@ 0014-4819
%C GERMANY
%K Adult
%K Comparative Study
%K Elbow Joint
%K Electromyography
%K Human
%K Linear Models
%K Male
%K Movement
%K Reaction Time
%K Support, Non-U.S. Gov't
%K Support, U.S. Gov't, Non-P.H.S.
%K Support, U.S. Gov't, P.H.S.
%K Viscosity
%K Weight-Bearing
%U http://biomednet.com/db/medline/98290367

%0 Journal Article
%1 98165876
%A Gribble, P.L.
%A Ostry, D.J.
%A Sanguineti, V.
%A Laboissiere, R.
%T Are complex control signals required for human arm movement?
%J J Neurophysiol
%V 79
%N 3
%P 1409-24
%D 1998
%O Department of Psychology, McGill University, Montreal, Quebec H3A 1B1,=
 Canada.
%X It has been proposed that the control signals underlying voluntary human=
 arm movement have a "complex" nonmonotonic time-varying form, and a number=
 of empirical findings have been offered in support of this idea. In this=
 paper, we address three such findings using a model of two-joint arm motion=
 based on the lambda version of the equilibrium-point hypothesis. The model=
 includes six one- and two-joint muscles, reflexes, modeled control signals,=
 muscle properties, and limb dynamics. First, we address the claim that=
 "complex" equilibrium trajectories are required to account for nonmonotonic=
 joint impedance patterns observed during multijoint movement. Using=
 constant-rate shifts in the neurally specified equilibrium of the limb and=
 constant cocontraction commands, we obtain patterns of predicted joint=
 stiffness during simulated multijoint movements that match the nonmonotonic=
 patterns reported empirically. We then use the algorithm proposed by Gomi=
 and Kawato to compute a hypothetical equilibrium trajectory from simulated=
 stiffness, viscosity, and limb kinematics. Like that reported by Gomi and=
 Kawato, the resulting trajectory was nonmonotonic, first leading then=
 lagging the position of the limb. Second, we address the claim that high=
 levels of stiffness are required to generate rapid single-joint movements=
 when simple equilibrium shifts are used. We compare empirical measurements=
 of stiffness during rapid single-joint movements with the predicted=
 stiffness of movements generated using constant-rate equilibrium shifts and=
 constant cocontraction commands. Single-joint movements are simulated at a=
 number of speeds, and the procedure used by Bennett to estimate stiffness=
 is followed. We show that when the magnitude of the cocontraction command=
 is scaled in proportion to movement speed, simulated joint stiffness varies=
 with movement speed in a manner comparable with that reported by Bennett.=
 Third, we address the related claim that nonmonotonic equilibrium shifts=
 are required to generate rapid single-joint movements. Using constant-rate=
 equilibrium shifts and constant cocontraction commands, rapid single-joint=
 movements are simulated in the presence of external torques. We use the=
 procedure reported by Latash and Gottlieb to compute hypothetical=
 equilibrium trajectories from simulated torque and angle measurements=
 during movement. As in Latash and Gottlieb, a nonmonotonic function is=
 obtained even though the control signals used in the simulations are=
 constant-rate changes in the equilibrium position of the limb. Differences=
 between the "simple" equilibrium trajectory proposed in the present paper=
 and those that are derived from the procedures used by Gomi and Kawato and=
 Latash and Gottlieb arise from their use of simplified models of force=
 generation.
%@ 0022-3077
%C UNITED STATES
%K Arm
%K Hand
%K Human
%K Joints
%K Mathematics
%K Models, Biological
%K Motor Activity
%K Movement
%K Muscle Contraction
%K Muscle, Skeletal
%K Reaction Time
%K Reflex
%K Support, Non-U.S. Gov't
%K Support, U.S. Gov't, P.H.S.
%U http://biomednet.com/db/medline/98165876

%0 Journal Article
%1 94275656
%A Bennett, D.J.
%T Stretch reflex responses in the human elbow joint during a voluntary=
 movement
%J J Physiol (Lond)
%V 474
%N 2
%P 339-51
%D 1994
%O Department of Brain and Cognitive Sciences, Massachusetts Institute of=
 Technology, Cambridge 01239.
%X 1. The responsiveness of the stretch reflex is modulated during human=
 voluntary limb movements. The influence of this modulation on the limb=
 mechanical properties (stiffness) was investigated. 2. Subjects were taught=
 to replicate accurately a rapid (4.0 rad s-1) targeted elbow flexion=
 movement of 1 rad. From the onset of 12% of the trials a sinusoidal=
 position disturbance (0.05 rad) was superimposed on the normal (trained)=
 movement trajectory. The net joint torque (muscle torque) resisting these=
 stretches was computed from measurements of applied torque, acceleration=
 and limb inertia. Electromyographic (EMG) responses in the triceps brachii=
 (TB), brachialis (Br) and biceps brachii (BB) were monitored. 3. The EMG=
 responses to sinusoidal stretches applied early in the movement were less=
 than those responses to perturbations applied when the arm neared the=
 target (especially in the antagonist muscle TB). These EMG responses caused=
 fluctuations in the resistance to the perturbation (stiffness), as=
 described below. 4. When the perturbation frequency was low (< 4 Hz) the=
 resistance of the elbow muscles to the stretch increased as the arm=
 approached the target (48% increase). In contrast, when the stretch=
 frequency was 7 Hz the resistance decreased by 63%. This decrease can be=
 explained by the increased reflex response, since at 7 Hz the reflex=
 response is probably timed so that it assists, rather than resists, the=
 stretching as a result of loop delays. This reflex timing was confirmed by=
 observing that, after abruptly stopping the sinusoidal stretch, the reflex=
 response persisted for 100 ms and was indeed in a direction that would have=
 reduced the resistance, had the perturbation continued. 5. The time course=
 of the net muscle stiffness was estimated for frequencies ranging from 4 to=
 8 Hz and for each 40 ms interval a Nyquist plot was constructed, forming a=
 C-shaped curve as frequency was varied. The size of this curve gave a=
 measure of the stiffness resulting from reflex activity. When the arm=
 neared the target this reflexive stiffness reached a maximum, and was=
 probably comparable in size to the intrinsic (non-reflexive) muscle=
 stiffness. Also, in four of the five subjects the viscous component of=
 stiffness at 7 Hz dropped significantly below zero when the arm neared the=
 target, again indicating that at this frequency the reflex was large and=
 acted inappropriately.(ABSTRACT TRUNCATED AT 400 WORDS)
%@ 0022-3751
%C ENGLAND
%K Adult
%K Elasticity
%K Elbow Joint
%K Electromyography
%K Female
%K Human
%K Male
%K Movement
%K Muscles
%K Reflex, Stretch
%K Support, Non-U.S. Gov't
%K Viscosity
%U http://biomednet.com/db/medline/94275656

%0 Journal Article
%1 86196249
%A Dingus, J.
%A Hwo, S.
%A Bryan, J.
%T Identification by monoclonal antibodies and characterization of human=
 platelet caldesmon
%J J Cell Biol
%V 102
%N 5
%P 1748-57
%D 1986
%X Actin-based gels were prepared from clarified high-salt extracts of human=
 platelets by dialysis against physiological salt buffers. The gel was=
 partially solubilized with 0.3 M KCl. Mice were immunized with the 0.3 M=
 KCl extract of the actin gel, and hybridomas were produced by fusion of=
 spleen cells with myeloma cells. Three hybridomas were generated that=
 secrete antibodies against an 80-kD protein. These monoclonal antibodies=
 stained stress fibers in cultured cells and cross-reacted with proteins in=
 several tissue types, including smooth muscle. The cross-reacting protein=
 in chicken gizzard smooth muscle had an apparent molecular weight of=
 140,000 and was demonstrated to be caldesmon, a calmodulin and=
 actin-binding protein (Sobue, K., Y. Muramoto, M. Fujita, and S. Kakiuchi,=
 Proc. Natl. Acad. Sci. USA, 78:5652-5655). No proteins of molecular weight=
 greater than 80 kD were=20detectable in platelets by immunoblotting using=
 the monoclonal antibodies. The 80-kD protein is heat stable and was=
 purified using modifications of the procedure reported by Bretscher for the=
 rapid purification of smooth muscle caldesmon (Bretscher, A., 1985, J.=
 Biol. Chem., 259:12873-12880). The 80-kD protein bound to=
 calmodulin-Sepharose in a Ca++-dependent manner and sedimented with actin=
 filaments, but did not greatly increase the viscosity of F-actin solutions.=
 The actin-binding activity was inhibited by calmodulin in the presence of=
 calcium. Except for the molecular weight difference, the 80-kD platelet=
 protein appears functionally similar to 140-kD smooth muscle caldesmon. We=
 propose that the 80-kD protein is platelet caldesmon.
%@ 0021-9525
%C UNITED STATES
%K Animal
%K Antibodies, Monoclonal
%K Blood Platelets
%K Calmodulin
%K Calmodulin-Binding Proteins
%K Carrier Proteins
%K Chickens
%K Fluorescent Antibody Technique
%K Gels
%K Gizzard
%K Human
%K Microfilament Proteins
%K Molecular Weight
%U http://biomednet.com/db/medline/86196249

%0 Journal Article
%1 86088110
%A Ravussin, P.
%A Archer, D.P.
%A Tyler, J.L.
%A Meyer, E.
%A Abou-Madi, M.
%A Diksic, M.
%A Yamamoto, L.
%A Trop, D.
%T Effects of rapid mannitol infusion on cerebral blood volume. A positron=
 emission tomographic study in dogs and man
%J J Neurosurg
%V 64
%N 1
%P 104-13
%D 1986
%X Positron emission tomography was used to study the effect of a rapid=
 infusion of mannitol on cerebral blood volume (CBV) in five dogs and in=
 three human subjects. The ability of mannitol to reduce intracranial=
 pressure (ICP) has always been attributed to its osmotic dehydrating=
 effect. The effects of mannitol infusion include increased osmolality,=
 total blood volume, central venous pressure (CVP), and cerebral blood flow,=
 and decreased hematocrit, hemoglobin concentration, serum sodium level, and=
 viscosity. Mannitol's ability to dilate the cerebral vasculature, either=
 directly or indirectly, and thus to transiently increase ICP, is a subject=
 of controversy. By in vivo labeling of red cells with carbon-11, the=
 authors were able to demonstrate an early increase in CBV in dogs of 20%,=
 27%, and 23% (mean increase, p less than 0.05) at 1, 2, and 3 minutes,=
 respectively, after an infusion of 20% mannitol (2 gm/kg over a 3-minute=
 period). The animals' muscle blood volume increased by 27% (mean increase,=
 p less than 0.05) 2 minutes after infusion. In the human subjects, lower=
 doses and a longer duration of infusion (1 gm/kg over 4 minutes) resulted=
 in an increase in CBV of 8%, 14% (p less than 0.05), and 10% at 1, 2, and 3=
 minutes, respectively, after infusion. In dogs, ICP increased by 4 mm Hg=
 (mean increase, p less than 0.05) 1 minute after the infusion, before=
 decreasing sharply. The ICP was not measured in the human subjects.=
 Hematocrit, hemoglobin, sodium, potassium, osmolality, heart rate, mean=
 arterial pressure (MAP), and CVP were measured serially. Results of these=
 measurements, as well as the significant decrease in MAP that occurred=
 after mannitol infusion, are discussed. This study demonstrated that rapid=
 mannitol infusion increases CBV and ICP. The increase in muscle blood=
 volume, in the presence of a decreased MAP and an adequate CVP, suggests=
 that mannitol may have caused vasodilation in these experiments.
%@ 0022-3085
%C UNITED STATES
%K Adult
%K Animal
%K Blood Pressure
%K Blood Volume
%K Brain
%K Dogs
%K Heart Rate
%K Human
%K Intracranial Pressure
%K Male
%K Mannitol
%K Middle Age
%K Potassium
%K Support, Non-U.S. Gov't
%K Tomography, Emission-Computed
%U http://biomednet.com/db/medline/86088110

--=====================_915460686==_
Content-Type: text/plain; charset="us-ascii"



*****************************************************************
Sladjan Milanovic              |    tel (+381 11) 685 788 ext 14
Institute for Medical Research |        (+381 11) 684 484 ext 14
Dr Subotica 4                  |    fax (+381 11) 643 691
PO BOX 721                     |    email:  milanos@imi.bg.ac.yu
11001 Belgrade                 |            milanos@ar.org.yu
Yugoslavia                     | 
*****************************************************************
--=====================_915460686==_--

