Publications by authors named "H Wendorf"

Purpose: The purpose of this proof of concept study is to demonstrate that electromyographic (EMG) activation patterns of leg muscles differ predictably among patients with predominantly spasticity, patients with predominantly dystonia, and typically developing control subjects during rest, volitional movement, and passively induced movement.

Methods: Eight control subjects, 6 subjects with dystonia, and 7 subjects with spasticity were recruited, ages 6-25 years. Surface EMG sensors were applied over 4 muscle groups of each leg.

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Aim: To examine the risk of obstructive sleep apnea (OSA) in children with cerebral palsy (CP) and/or epilepsy.

Method: This cross-sectional study employs the Pediatric Sleep Questionnaire (PSQ), the Gross Motor Function Classification System (GMFCS), and chart review to identify symptoms of OSA in children presenting to a multi-specialty pediatric healthcare institution.

Results: Two-hundred and fifteen patients were grouped into those with epilepsy (n=54), CP (n=18), both (n=55), and neither (comparison group, n=88).

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This randomized, double-blind, placebo-controlled study compared the efficacy of inhaled nitrous oxide (N(2)O) with enteral midazolam for sedation of children with cerebral palsy (CP) undergoing botulinum toxin A (BoNT-A) injections. Fifty children (29 males, 21 females; mean age 8y 2mo [SD 4y 5mo]; range 1-16y) were randomized to sedation with N(2)O (n=25) or midazolam (n=25). Groups were similar in type of CP (diplegia, 11; triplegia, three; quadriplegia, 16; hemiplegia, 16; other, three) and Gross Motor Function Classification System level (Level I, 4; II, 24; III, 4; IV, 13; V, 5).

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Here we provide experimental evidence that identifies JAK3 as one of the regulators of platelet function. Treatment of platelets with thrombin induced tyrosine phosphorylation of the JAK3 target substrates STAT1 and STAT3. Platelets from JAK3-deficient mice displayed a decrease in tyrosine phosphorylation of STAT1 and STAT3.

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We evaluated the TXU (anti-CD7)-pokeweed antiviral protein (PAP) immunotoxin in both murine and nonhuman primate models. TXU-PAP caused dose-limiting cardiac toxicity in BALB/c mice. In a SCID mouse model of invariably fatal human T-lineage acute lymphoblastic leukemia (ALL), TXU-PAP therapy resulted in a marked improvement of leukemia-free survival without any side effects.

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