Browsing by Subject "gait"

Now showing 1 - 2 of 2

Open Access
Human motion control using inverse kinematics
(2003) Memişoğlu, Aydemir
Articulated figure animation receives particular attention of the computer graphics society. The techniques for animation of articulated figures range from simple interpolation between keyframes methods to motion-capture techniques. One of these techniques, inverse kinematics, which is adopted from robotics, provides the animator the ability to specify a large quantity of motion parameters that results with realistic animations. This study presents an interactive hierarchical motion control system used for the animation of human figure locomotion. We aimed to develop an articulated figure animation system that creates movements , like goal-directed motion and walking by using motion control techniques at different levels. Inverse Kinematics using Analytical Methods (IKAN) software, which was developed at the University of Pennsylvania, is utilized for controlling the motion of the articulated body using inverse kinematics.
Open Access
Mutations in the very low-density lipoprotein receptor VLDLR cause cerebellar hypoplasia and quadrupedal locomotion in humans
(National Academy of Sciences, 2008) Ozcelik, T.; Akarsu, N.; Uz, E.; Caglayan, S.; Gulsuner, S.; Onat, O. E.; Tan, M.; Tan, U.
Quadrupedal gait in humans, also known as Unertan syndrome, is a rare phenotype associated with dysarthric speech, mental retardation, and varying degrees of cerebrocerebellar hypoplasia. Four large consanguineous kindreds from Turkey manifest this phenotype. In two families (A and D), shared homozygosity among affected relatives mapped the trait to a 1.3-Mb region of chromosome 9p24. This genomic region includes the VLDLR gene, which encodes the very low-density lipoprotein receptor, a component of the reelin signaling pathway involved in neuroblast migration in the cerebral cortex and cerebellum. Sequence analysis of VLDLR revealed nonsense mutation R257X in family A and single-nucleotide deletion c2339delT in family D. Both these mutations are predicted to lead to truncated proteins lacking transmembrane and signaling domains. In two other families (B and C), the phenotype is not linked to chromosome 9p. Our data indicate that mutations in VLDLR impair cerebrocerebellar function, conferring in these families a dramatic influence on gait, and that hereditary disorders associated with quadrupedal gait in humans are genetically heterogeneous.