Biomedical subjects

R Cavazos

Publications and source records attributed to R Cavazos.

6 recordsLinked to original sources

PubMed1994

Contextual interference effects with skilled baseball players.

The learning benefits of contextual interference have been frequently demonstrated in different settings using novice learners. The purpose of the present study was to test such effects with skilled athletic performers. Scheduling differences for biweekly additional ("extra") batting-practice sessions of a collegiate baseball team were examined. 30 players (ns = 10) were blocked on skill and then randomly assigned to one of three groups. The random and blocked groups received 2 additional batting-practice sessions each week for 6 wk. (12 sessions), while the control group received no additional practice. The extra sessions consisted of 45 pitches, 15 fastballs, 15 curveballs, and 15 change-up pitches. The random group received these pitches in a random order, while the blocked group received all 15 of one type, then 15 of the next type, and finally 15 of the last type of pitch in a blocked fashion. All subjects received a pretest of 45 randomly presented pitches of the three varieties. After 6 wk. of extra batting practice, all subjects received two transfer tests, each of 45 trials; one was presented randomly and one blocked. The transfer tests were counterbalanced across subjects. Pretest analysis showed no significant differences among groups. On both the random and blocked transfer tests, however, the random group performed with reliably higher scores than the blocked group, who performed better than the control group. When comparing the pretest to the random transfer test, the random group improved 56.7%, the blocked group 24.8%, and the control group only 6.2%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1990

Metabolism of methacrylonitrile to cyanide: in vitro studies.

In liver fractions from male Sprague-Dawley rats, the metabolism of methacrylonitrile (MeAN) to cyanide (CN-) was localized in microsomal fraction and required reduced nicotinamide adenine dinucleotide phosphate (NADPH) and oxygen for maximal activity. The biotransformation of MeAN to CN- was characterized with respect to time, microsomal protein concentration, pH, and temperature. Metabolism of MeAN was increased in microsomes obtained from phenobarbital-treated rats (310% of control) and decreased with CoCl2 and SKF 525 A treatments (55% and 61%, respectively). Addition of the epoxide hydratase inhibitor, 1,1,1-trichloropropane 2,3-oxide, decreased the formation of CN- from MeAN. Addition of glutathione, cysteine, D-penicillamine, and 2-mercaptoethanol enhanced the released of CN- from MeAN. These findings indicate that MeAN is metabolized to CN- via a cytochrome P-450-dependent mixed-function oxidase system.

Animals↗

PubMed1990

Toxicity and tissue distribution of methacrylonitrile in rats.

The toxicity, uptake, tissue distribution, elimination, and covalent binding of 2-[14C]methyl-[2.3-14C]acrylonitrile (MeAN) in male Sprague-Dawley rats were investigated. Following an oral administration of 100 mg/Kg body weight (0.5 LD50, 8 microCi/Kg bw) the rats exhibited several signs of toxicity including ataxia, convulsions, mild diarrhea, salivation, lacrimation, and bladder urine retention. The treated animals excreted 43% of the 14C in the urine, 14% in the feces, and 2.5% in the expired air as 14CO2 in 10 days. Hydrogen cyanide was not detectable. Red blood cells retained significant amounts of radioactivity for more than 10 days after treatment. MeAN was extensively absorbed through the gastrointestinal tract and distributed in all the tissues of the rats. The major concentrations of the radioactivity were found with up to 25% of the administered dose in bone, liver, spleen, kidney, blood, and the gastrointestinal tract. This study indicates that MeAN is rapidly absorbed and distributed and the major route of excretion is urinary.

Air↗

PubMed1989

Disposition of methacrylonitrile in rats and distribution in blood components.

The interaction of 2[14C]methyl-2,3[14C]acrylonitrile (MeAN) with the components of blood and its disposition in male Sprague-Dawley rats has been investigated. Following an oral administration of 100 mg/kg (0.5 LD50, 8 microCi/kg), the rats excreted 43% of the [14C] in the urine, 15% in the feces and 2.5% in the expired air as 14CO2 in 5 days. Hydrogen cyanide (H14CN) was not detectable. The red blood cells retained significant amounts of radioactivity for more than five days after administration, whereas the [14C]-activity in plasma declined sharply. More than 50% of the radioactivity in erythrocytes was detected as covalently bound to cytoplasmic (hemoglobin) and membrane proteins. A small amount of radioactivity was also found in the heme fraction. About 13% of the total dose administered was recovered as thiocyanate in the plasma and the urine. These results suggest that the toxicity of MeAN may be attributable to the whole molecule and not entirely to the in vivo liberation of cyanide.

Acrylates↗

PubMed1988

Interaction of methacrylonitrile with glutathione.

The interaction of methacrylonitrile (MeAN) with glutathione (GSH) was evaluated in aqueous solution and its in vivo potential to deplete GSH in male Sprague Dawley rats at the 0.5 LD50 dose of 100 mg MeAN/Kg body weight was investigated. Addition of MeAN (0-40 mM) to a solution of 0.3 mM GSH in 2 mM EDTA, pH 7.4, resulted in a time and concentration dependent depletion of GSH determined as nonprotein sulfhydryl. Thin layer chromatography analysis of incubation mixtures of MeAN with GSH and cysteine showed the appearance of distinct spots representing the adducts S-cyanopropyl GSH and S-cyanopropyl cysteine. Oral administration of MeAN to the rats resulted in significant depletion of GSH in the liver, kidney, heart, lung, brain and spleen. The maximum GSH depletion was noticed in the liver (approximately 39% of control) and in other organs it ranged between 26-34% of control. It is likely that the toxicity of MeAN may be related to in vivo GSH depletion.

Acrylates↗

PubMedDate not supplied

[Reye's syndrome in an adult. Review of pathogenic mechanisms].

Reye's syndrome is considered a disease of the pediatric age. It is characterized by a prodrome of viral illness followed by vomiting and encephalopathy with associated hepatic dysfunction. This syndrome is potentially life-threatening with high morbidity and mortality rates. There are 27 other cases of adult onset Reye's syndrome reported in the literature. We describe a 18-year-old woman who developed varicella and four days later started with vomiting, delirium and in the following day she became comatose. Laboratory tests of liver function and pathology of a liver biopsy proved the diagnosis. The patient survived. A review of the proposed pathogenic mechanisms are presented. Our patient represents case the number 28 in world literature and the first in the mexican literature.

Adolescent↗