“
“Study design: Intervention study.

Objectives: The present study aimed at examining whether spinal and/or peripheral alterations are in the origin of neuromuscular fatigue development induced by intermittent neuromuscular electrical stimulation (NMES) in subjects with complete spinal cord injury (SCI).

Setting: Neurological Rehabilitation Center CMN Propara, Montpellier, France.

Methods: Thirteen volunteers with complete SCI participated in the study. The right triceps surae muscle was fatigued using a 30-Hz NMES protocol (2 s ON-2 s OFF) composed of three series of five trains. Selleck SYN-117 Spinal excitability (assessed by the H-reflex), muscle excitability (assessed by the

M-wave), muscle contractile properties (assessed by mechanical response parameters) and torque evoked by NMES were tested before and after each five-train series.

Results: NMES-evoked torque significantly decreased throughout the protocol (P<0.001). This decrease was accompanied by a significant increase in M-wave amplitude (P<0.001), whereas H-reflex and the H-max/M-max ratio were not significantly modified. The amplitude of the mechanical response was significantly decreased at the end of the protocol

(P<0.05).

Conclusion: The results indicate significant fatigue development, which was attributed to impaired cross-bridge force-generating capacity, without modification of spinal excitability nor muscle excitability.”
“The

aim of the study was to assess the activity of AP-1 family proteins, e.g. Fra-1, Fra-2, JunB, JunD, and FosB, selleck kinase inhibitor engaged in the regulation of inducible nitric oxide synthase 3-MA in vivo (iNOS) expression and the production of NO by neutrophils (PMN) exposed to N-nitrosodimethylamine (NDMA) xenobiotic. Isolated human PMN were incubated in the presence of NDMA. iNOS mRNA expression was then analyzed using Northern blot and the expression of other proteins in the cytoplasmic and nuclear fractions were assessed using Western blot. The obtained results indicate that NDMA increased iNOS mRNA and protein expression in human PMN. Furthermore, it increased the expression of Fra-1, Fra-2, JunB, and JunD in the cytoplasmic fraction, and FosB expression in the fractions of analyzed cells. As a consequence of inhibiting p38 pathway and JNK, reduced iNOS expression and NO production was noted in PMN exposed to NDMA. Inhibition of the p38 pathway resulted in reduced expression of all analyzed proteins in the cytoplasmic fraction of PMN exposed to NDMA. Furthermore, increased Fra-2 expression and reduced FosB expression were found in the nuclear fraction of those cells. Inhibiting ERK5 pathway resulted in increased JunB expression in both fractions of the analyzed cells. Therefore, no changes in the expression of analyzed proteins in the presence of NDMA were observed in PMN pre-incubated with JNK pathway inhibitor.