1 s were consistent with a mechanism of forced hyperextension.

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

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

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

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

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

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

8                                              Hyperextension-induced hypoalgesia terminated immediatel

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

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

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

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

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