1 ension or lumbosacral plexus injury from leg hyperextension.

2 er, or at 30 and 60 s following milk-induced hyperextension.

3 s were consistent with a mechanism of forced hyperextension.

4 in walls, which provide geometric control of hyperextension.

5      The loss of V2b INs results in hindlimb hyperextension and a delay in the transition from stance

6 VI based on injury mechanism (e.g., cervical hyperextension) and injury patterns (e.g., cervical and

7 of generalized rigidity and myoclonus, axial hyperextension, and trismus, without impairment of consc

8  five out of six subjects had decreased knee hyperextension at the post-training session (on average

9 -infant interactions, contact, suckling, and hyperextension during milk letdown, cause varying degree

10 , n = 6) or absence (group B, n = 8) of knee hyperextension during stance phase of walking.

11 y being that of stretch injury from cervical hyperextension/flexion.

12                                              Hyperextension-induced hypoalgesia terminated immediatel

13 tal limits of cellular deformations, such as hyperextension of a living cell, remain poorly understoo

14 n preventing excessive external rotation and hyperextension of the knee.

15                          This results from a hyperextension of the ligand binding core compared with

16 t the binding of UBP282 produces the largest hyperextension of the lobes yet reported for an AMPA rec

17 neous breaking of the D1 dimer interface and hyperextension of the lower lobes of the ligand binding

18                                              Hyperextension of the margin occurred only at activation

19                                         This hyperextension resulted in a 34-fold asymmetry in the ci

20 leton and membrane architecture that enables hyperextensions through the folding and unfolding of cel

21 dlimb movements and postures when awake, and hyperextension when asleep.