Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.21 (CPT)
 4,580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subjects performed 9 wk of isokinetic knee extensions twice weekly. Albuterol (N = 13) or placebo (N = 9) was administered for 6 wk; groups received 16 mg.d-1 of either treatment. Training consisted of three sets of 10 repetitions at 45 degrees.s-1. Data were collected at weeks 0, 6, and 9. Concentric and eccentric variables examined included: peak torque (CPT, EPT), total work (CTW, ETW), average power (CAP, EAP), time to peak torque (CTTPT, ETTPT), peak torque to body weight ratio (CPT/BW), and work to body weight ratio (CW/BW, EW/BW). Other variables included: thigh circumference (CIRC), thigh cross-sectional area (CSA), forced vital capacity (FVC), and forced expiratory volume (FEV1), MANOVA and the Dunn-Bonferroni post-hoc found differences within groups for CPT, CTW, CAP, CPR/BW, EPT, ETTPT, and CSA. Interactions were noted for CW/BW, ETW, EAP, EPT/BW, and ETW/BW; with persons administered albuterol yielding superior values. CW/BW, ETW, and EAP showed interactions at post-testing, while EPT/BW and EW/BW interacted at both midtesting and post-testing. Results indicate therapeutic doses of albuterol administered with resistance exercise may augment strength gains.
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PMID:The effects of albuterol and isokinetic exercise on the quadriceps muscle group. 858 82

Stabilization of the avicide 3-chloro-p-toluidine (CPTH) on rice baits by pseudo latex polymeric coating and beta-cyclodextin inclusion was investigated. When CPTH-treated rice baits were exposed to sunlight, the CPTH formed colored compounds, which exacerbated problems with bait acceptance and efficacy. Fluidized bed coating with controlled-release polymeric psuedo latexes (RS, RL, NE) reduced CPTH loss but did not eliminate color formation. Enteric pseudo latex coatings (CAP and 4110) gave mixed results. Coating 4110 reduced CPTH loss but still allowed color formation, whereas CAP allowed more CPTH loss than any other coating as well as increased color formation. Inclusion in beta-cyclodextrin (molar ratio 1:1) led to enhanced retention of CPTH and minimal color formation. The CPT/beta-cyclodextrin adduct increased retention of CPTH from 43 to 70% upon simulated weathering. The retention was independent of the adhesives used for attachment.
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PMID:Stabilization of the avicide 3-chloro-p-toluidine as the beta-cyclodextrin adduct. 1055 84

Capsaicin, the pungent ingredient in hot pepper, activates nociceptors to produce pain and inflammation. However, repeated exposures of capsaicin will cause desensitization to nociceptive stimuli. In cultured trigeminal ganglion (TG) neurons, we investigated mechanisms underlying capsaicin-mediated inhibition of action potentials (APs) and modulation of voltage-gated sodium channels (VGSCs). Capsaicin (1 microM) inhibited APs and VGSCs only in capsaicin-sensitive neurons. Repeated applications of capsaicin produced depolarizing potentials but failed to evoke APs. The capsaicin-induced inhibition of VGSCs was prevented by preexposing the capsaicin receptor antagonist, capsazepine (CPZ). The magnitude of the capsaicin-induced inhibition of VGSCs was dose dependent, having a K(1/2) = 0.45 microM. The magnitude of the inhibition of VGSCs was proportional to the capsaicin induced current (for -I(CAP) < 0.2 nA). Capsaicin inhibited activation of VGSCs without changing the voltage dependence of activation or markedly changing channel inactivation and use-dependent block. To explore the changes leading to this inhibition, it was found that capsaicin increased cAMP with a K(1/2) = 0.18 microM. At 1 microM capsaicin, this cAMP generation was inhibited 64% by10 microM CPZ, suggesting that activation of capsaicin receptors increased cAMP. The addition of 100 microM CPT-cAMP increased the capsaicin-activated currents but inhibited the VGSCs in both capsaicin-sensitive and -insensitive neurons. In summary, the inhibitory effects of capsaicin on VGSCs and the generation of APs are mediated by activation of capsaicin receptors. The capsaicin-induced activation of second messengers, such as cAMP, play a part in this modulation. These data distinguish two pathways by which neuronal sensitivity can be diminished by capsaicin: by modulation of the capsaicin receptor sensitivity, since the block of VGSCs is proportional to the magnitude of the capsaicin-evoked currents, and by modulation of VGSCs through second messengers elevated by capsaicin receptor activation. These mechanisms are likely to be important in understanding the analgesic effects of capsaicin.
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PMID:Capsaicin inhibits activation of voltage-gated sodium currents in capsaicin-sensitive trigeminal ganglion neurons. 1116 May 9