RESUMO
The purpose of this study was to compare the acute effects of general, specific and combined warm-up (WU) on explosive performance. Healthy male (n = 10) subjects participated in six WU protocols in a crossover randomized study design. Protocols were: passive rest (PR; 15 min of passive rest), running (Run; 5 min of running at 70% of maximum heart rate), stretching (STR; 5 min of static stretching exercise), jumping [Jump; 5 min of jumping exercises - 3x8 countermovement jumps (CMJ) and 3x8 drop jumps from 60 cm (DJ60)], and combined (COM; protocols Run+STR+Jump combined). Immediately before and after each WU, subjects were assessed for explosive concentric-only (i.e. squat jump - SJ), slow stretch-shortening cycle (i.e. CMJ), fast stretch-shortening cycle (i.e. DJ60) and contact time (CT) muscle performance. PR significantly reduced SJ performance (p =0.007). Run increased SJ (p =0.0001) and CMJ (p =0.002). STR increased CMJ (p =0.048). Specific WU (i.e. Jump) increased SJ (p =0.001), CMJ (p =0.028) and DJ60 (p =0.006) performance. COM increased CMJ performance (p =0.006). Jump was superior in SJ performance vs. PR (p =0.001). Jump reduced (p =0.03) CT in DJ60. In conclusion, general, specific and combined WU increase slow stretch-shortening cycle (SSC) muscle performance, but only specific WU increases fast SSC muscle performance. Therefore, to increase fast SSC performance, specific fast SSC muscle actions must be included during the WU.
RESUMO
BACKGROUND: Tumor necrosis factor antagonists are useful in the treatment of several chronic inflammatory immune mediated diseases. AIM: To assess the effects of infliximab in 21 patients with inflammatory arthropaties, refractary to conventional treatment. PATIENTS AND METHODS: Eleven patients with rheumatoid arthritis, seven with psoriatic arthritis and three with spondyloarthritis were treated. The mean duration of the diseases was 10 years. Infliximab was administered intravenously in a dose of 3 mg/kg body weight. A median of 6 doses in 8 months was administered. Effectiveness was assessed in 19 patients that received three or more doses. RESULTS: Infliximab was effective in 16 patients (10 with rheumatoid arthritis, four with psoriasis and two with spondyloarthritis) and ineffective in three. In responsive patients, a reduction in the number of inflammed joints and morning stiffness and an improvement in functional capacity was observed. Fifteen of the 16 patients perceived an improvement in their health status. This answer was concordant with concomitant medical evaluation in 15. Patients that maintained the treatment felt very well, well or regular, whereas five of six patients that discontinued the treatment felt ill. Thirteen patients had adverse effects. Treatment was discontinued in two patients due to drug induced lupus, allergy in 2, hypertension in one, high costs in three and lack of response in three. CONCLUSIONS: Infliximab reduced arthritic activity in 16 of 19 patients with severe treatment refractary arthritis.
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Antirreumáticos , Anticorpos Monoclonais/uso terapêutico , Artrite/tratamento farmacológico , Fator de Necrose Tumoral alfa , Artrite Psoriásica/tratamento farmacológico , Artrite Reumatoide/tratamento farmacológico , Espondilartrite/tratamento farmacológico , Resistência a Medicamentos , Resultado do TratamentoRESUMO
Phencyclidine (PCP) is a non-competitive inhibitor of the nicotinic acetylcholine receptor (nAChR) with biphasic characteristics. At low and high micromolar concentrations, PCP inhibits nAChR from fetal mouse muscle, whereas at intermediate concentrations PCP does not inhibit the receptor. The present study was performed to determine whether the high and low concentration effects of PCP on mouse nAChR were due to interactions of this blocker with channel lining amino acids. In order to test this hypothesis, we examined the ability of PCP to inhibit acetylcholine-induced currents from wild-type nAChR and nAChR in which amino acid substitutions were made in the 6', 8' and 10' positions of the M2 transmembrane segments of the receptor. Fetal mouse nAChR from BC(3)H-1 cells were expressed in Xenopus laevis oocytes and studied using the two-electrode voltage clamp technique. The results of this study reveal that in native fetal muscle receptor, PCP potency is not affected by membrane potential between -80 mV and -30 mV. The potency of PCP is increased by mutations in M2 6', 8', and 10' positions. This increase in potency cannot be explained merely by either changes in hydrophobicity/hydrophilicity of amino acids at these positions or by side-chain size. A model proposing extra-luminal inhibitory and regulatory sites for PCP explains the lack of voltage-dependency, the biphasic effect of PCP, and the fact that all M2 mutations increased PCP potency (by disrupting the link with the regulatory sites).