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Retinoic acid-binding protein is present in metastatic murine colon tumors as well as in Lewis lung tumors and in lungs and brains of mice bearing these tumors; however, this protein is below the limits of detection in weakly-metastatic carcinomas and in normal lung, colon, or brains. These observations are interesting since they concern the possibility of measuring the binding protein levels of colon tumors in clinical specimens as biochemical markers in human malignancy. A total of thirty-three human colon tumors and related materials were analyzed for the presence of the binding protein. The interfering serum albumin, which nonspecifically binds retinoic acid, was eliminated by affinity chromatography. Of the twenty colon, cecum, and rectum tumors analyzed, 80% contained the binding protein in detectable amounts, and 20% showed nondetectable or marginally detectable amounts. Twenty-two percent of the human colon segments isolated from patients suspected for colon tumors contained the binding protein in readily detectable amounts, whereas 78% revealed nondetectable to marginally detectable amounts. The retinoic acid-binding protein of human colon tumor shared the same ligand specificity, thiol functions in ligand-binding, and sedimentation coefficient as the binding protein isolated from chick embryo skin. However, the human protein exhibited altered isoelectric pH.

Hemiparetic gait is characterized by slow speed and poorly coordinated movements. Because the values of gait parameters vary with changes in speed, the slow speed that is typical of hemiparetic gait necessitates applying controls for the influence of speed when comparing hemiparetic and able-bodied persons. Gait kinetics and kinematics were measured in seven hemiparetic and seven able-bodied adults to compare their gait patterns at similar speeds and to assess the effectiveness of ankle-foot orthoses which were double-stopped in 5 degrees of dorsiflexion or 5 degrees of plantarflexion. Hemiparetic persons ambulating without the orthoses had a shorter step length, longer duration stance, and shorter duration swing than normal. They displayed greater than normal flexion of the affected hip during midstance, which, by putting the center of mass farther in front of the knee, may explain the increased knee extension moment due to vertical force. Affected hip adduction during single support was less in hemiparetic persons than in able-bodied persons, indicating a decreased lateral shift to the paretic side. During the swing phase, the affected limbs of hemiparetic persons were in less knee flexion and less dorsiflexion than normal, necessitating circumduction to achieve toe clearance. Ankle-foot orthoses increased walking speed to normalize heelstrike duration through use of an optimally adjusted plantarflexion stop. An improperly adjusted orthosis may produce an exaggerated knee flexion moment resulting in knee instability.

Stroke, brain injury, incomplete spinal cord injuries, and peripheral neuropathies frequently result in dysfunction of the foot dorsiflexors and evertors. A controlled examination of aspects of these disabilities was conducted with normal volunteers who underwent a temporary peroneal nerve block. The effects of peroneal nerve paralysis were analyzed to quantitatively describe the resulting gait abnormalities and to assess the effectiveness of orthoses in restoring a normal gait pattern. Kinematic and kinetic measurements were made during normal ambulation, ambulation with a right peroneal nerve paralysis, and ambulation with a paralysis and an ankle-foot orthosis (AFO) with three different adjustments: a posterior stop set in 5 degrees plantarflexion, a posterior stop set in 5 degrees dorsiflexion, and spring-assisted dorsiflexion. The peroneal paralysis produced abnormalities during both the stance and swing phases of gait. During early stance there was a decrease in the length of the heelstrike phase and a reduction in the peak plantarflexion moment (p less than 0.01). During midstance there was an increase in the range of inversion-eversion achieved suggesting medial-lateral instability (p less than 0.01). The second vertical force peak and the aft-shear force peak were reduced (p less than 0.05) as were the peak dorsiflexion moment and the opposite steplength (p less than 0.01). These reductions are believed to be due to medial-lateral instability during pushoff. Subjects demonstrated a steppage gait during swing phase and increased inversion just prior to heelstrike (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Gastrocnemius-soleus dysfunction is a frequent result of cauda equina lesions and peripheral neurophathies and of stroke and brain injury. Temporary tibial nerve paralysis constitutes a comparable laboratory condition which allows the controlled examination of aspects of these disabilities. The biomechanical effects of temporary tibial nerve paralysis in six normal young adult volunteers were examined to quantitatively define the gait abnormalities resulting from gastrocnemius-soleus paralysis and to provide a basis for the assessment of the effectiveness of different orthotic designs in restoring a normal gait pattern. The motion of the right lower extremity, ground reactive forces acting on the right lower extremity, timing of gait events and step length were recorded, first during normal ambulation and then during ambulation after a right tibial nerve block. Step length was reduced bilaterally after the nerve block (p less than 0.005); the reduction was greater for the left (unblocked) step than for the right (blocked) step (p less than 0.005). Right heeloff was delayed until the time of left heelstrike in all subjects after the right tibial block. Right heeloff occurred later (p less than 0.005) while left heelstrike occurred earlier than normal (p less than 0.005). The shorter left step length and earlier left heelstrike resulted from a reduction in the forward progression of the right hip (p less than 0.001). When subjects were deprived of the plantarflexion activity necessary to counteract dorsiflexion moments at the ankle, they delayed the forward progression of the center of pressure (p less than 0.001) to avoid the unstable collapse of the foot into dorsiflexion.(ABSTRACT TRUNCATED AT 250 WORDS)

Retinoic acid-binding protein is present in metastatic murine colon tumors as well as in Lewis lung tumors and in lungs and brains of mice bearing these tumors; however, this protein is below the limits of detection in weakly-metastatic carcinomas and in normal lung, colon, or brains. These observations are interesting since they concern the possibility of measuring the binding protein levels of colon tumors in clinical specimens as biochemical markers in human malignancy. A total of thirty-three human colon tumors and related materials were analyzed for the presence of the binding protein. The interfering serum albumin, which nonspecifically binds retinoic acid, was eliminated by affinity chromatography. Of the twenty colon, cecum, and rectum tumors analyzed, 80% contained the binding protein in detectable amounts, and 20% showed nondetectable or marginally detectable amounts. Twenty-two percent of the human colon segments isolated from patients suspected for colon tumors contained the binding protein in readily detectable amounts, whereas 78% revealed nondetectable to marginally detectable amounts. The retinoic acid-binding protein of human colon tumor shared the same ligand specificity, thiol functions in ligand-binding, and sedimentation coefficient as the binding protein isolated from chick embryo skin. However, the human protein exhibited altered isoelectric pH.

Subjects performed the Brooks (1967) spatial and nonspatial memory tasks either while sitting or while maintaining a difficult standing balance position. The balance task disrupted spatial but not nonspatial memory performance. Balance steadiness during spatial and nonspatial memory conditions did not differ. These results suggest that cognitive spatial processing may rely on neural mechanisms that are also required for the regulation of posture.