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Biomedical subjects

D Vazquez

Publications and source records attributed to D Vazquez.

At least 19 recordsLinked to original sources
PubMed2002

Cortical neuronal ensembles driven by dorsal horn spinal neurones with spontaneous activity in the cat.

Simultaneous recordings of cortical activity, recorded as the cortical local field potential (CLFP) in the contralateral posterior sigmoid gyrus, and the spinal activity, recorded as the cord dorsum potential (CDP) of the L6 lumbar segment, were made in the anaesthetized cat. The electrodes were positioned in somatosensory regions where the largest spontaneous negative CLFPs and CDPs were recorded. We found that spontaneous negative CLFPs were preceded by spontaneous negative CDPs with a mean latency of 14.4+/-3.5 ms. Amplitude of these spontaneous negative CLFPs was abolished after section of the dorsal columns and ipsilateral dorsolateral funiculus. It is concluded that the neurones of the primary somatosensory cortex can be driven by dorsal horn spinal neurones producing the spontaneous negative CDPs. This suggests very strongly that spontaneous neuronal activity in somatosensory regions of the brain is generated not only by ongoing activity of neurones located at supraspinal sites, but also by ongoing activity of spinal neurones.

Action Potentials↗
PubMed2000

Altered response to partial bladder outlet obstruction in mice lacking inducible nitric oxide synthase.

INTRODUCTION: Following prolonged partial bladder outlet obstruction (BOO) in the mouse, cholinergic mediated detrusor contractility decreases. Previous work has demonstrated an increase in the inducible form of nitric oxide synthase (iNOS) at the mRNA and protein levels soon after obstruction. Since nitric oxide (NO), the product of the action of iNOS on molecular oxygen and l-arginine, produces vasodilation and decreases platelet aggregation, we believe it is an integral part of the initial detrusor response to obstruction. These experiments evaluated the detrusor response in mice incapable of producing iNOS. MATERIALS AND METHODS: Wild type and knockout mice were partially obstructed for 1, 3, and 5 weeks. Physiologic evaluation consisted of cystometric analyses, and muscle strip studies in response to cholinergic and electrical stimulation. Strips were also relaxed with L-arginine, sodium nitroprusside, and 8-bromoguanosine 3' - 5' cyclic GMP, after precontraction. RESULTS: After 5 weeks of obstruction, both wild type (WT) and knockout (KO) mouse bladders increased significantly in weight. WT bladders obstructed for 5 weeks had the greatest capacity (increase of 42%, p = 0.022), and a decreased contractile response to carbachol (decrease of 32% at 10-5 M, p = 0.018). No differences were noted at 1 and 3 weeks of obstruction. In contrast, KO mice had a significantly larger bladder capacity at 1 week of obstruction compared with WT, and had significantly lower responses to electrical stimulation than WT at the same time (p = 0.03). Additionally, after 5 weeks of obstruction, bladder capacity and contractility returned to baseline levels in KO mice, at a time when WT mice had significantly larger capacity and decreased contractility. CONCLUSIONS: Bladder function following partial BOO in mice incapable of producing iNOS differed significantly from the normal response. Our data suggest that generation of iNOS soon after obstruction is necessary to prevent detrusor dysfunction at that time. Moreover, the enhanced function seen in KO bladders after longer periods of obstruction (5 weeks) in comparison to WT bladders suggests that reactive nitrogen species-induced protein nitrosylation may be involved in the loss of contractile function observed after more prolonged periods of obstruction.

Animals↗
PubMed1996

Hypercortisolemia, hippocampal glucocorticoid receptors, and fast feedback.

Glucocorticoids are critical for survival. The absence of glucocorticoids leads to the inability of the organism to cope with stress and subsequent death. However, diseases of glucocorticoid excess, such as Cushing's disease, make it clear that 'too much circulating glucocorticoids is also bad.' The need to control the circulating levels of glucocorticoids to prevent oversecretion leads to an elaborate set of checks and balances, in particular, the levels of glucocorticoid 'feedback' to the controlling elements to turn off glucocorticoid secretion and consequently maintain the homeostatic range of glucocorticoids. In order to accomplish these goals, multiple types of feedback exist which appear to use different intracellular mechanisms. In addition to multiple types of feedback, there are multiple sites of feedback including numerous limbic areas that influence the inhibition of the stress response. In this article, we will discuss the role of hippocampal limbic circuits in modulation of the stress response and the evidence which support the theory that changes in these circuits are associated with feedback abnormalities. We will review studies in humans which suggest that damage to the hippocampus can lead to changes in glucocorticoid feedback, and finally we will review the evidence that glucocorticoids themselves can lead to changes in hippocampal neurons resulting in feedback abnormalities.

Feedback↗
PubMed1994

Thoracic disc herniation, cord compression, and paraplegia caused by electrical injury: case report and review of the literature.

The case of a patient with thoracic intervertebral disc prolapse, cord compression, and delayed paraplegia with recovery secondary to high-tension electrical current is presented. The unusual entry wound in the neck, makes this a rare event that to our knowledge has not been previously described in the literature. Magnetic resonance imaging allowed noninvasive and early diagnosis, and in the future probably will reveal the true incidence of cord compression in electrical injury victims.

Adult↗
PubMed1990

Carbamazepine metabolism in humans: effect of concurrent anticonvulsant therapy.

Free and total carbamazepine (CBZ) and carbamazepine-epoxide (CBZ-EP) plasma levels were obtained on 113 patients with epilepsy (18-61 years old) controlled on either monotherapy or coadministration with either phenobarbital (PB), phenytoin (PHT), valproic acid (VPA), or all three. A subset of patients were administered tetradeuterium labeled CBZ to evaluate the effects of autoinduction and coadministration of VPA on the kinetics of CBZ and its metabolite CBZ-EP. Polytherapy had variable effect on free and total CBZ plasma levels compared to monotherapy. Coadministered PHT (co-PHT), or all three anticonvulsants together (PHT, PB, and VPA: co-AEDs) decreased free and total CBZ plasma levels. No change was noted for coadministered VPA (co-VPA). Compared to monotherapy the free and total CBZ-EP levels increased with co-VPA, less with coadministered PB (co-PB), and no change with co-PHT or co-AEDs. Protein binding of CBZ and CBZ-EP was not affected by any antiepileptic drugs studied. The free and total CBZ-EP/CBZ ratio was tripled with co-VPA or co-AED's, and doubled with co-PHT or co-PB. Isotope labeling did not demonstrate any differences in half-life (t1/2), plasma clearance (Cl), or volume of distribution (Vd). Compared to naive controls, monotherapy and co-VPA decreased CBZ t1/2 by 50%, and more than doubled the CBZ Cl without a significant change in the Vd. Autoinduction is one explanation for these changes with chronic CBZ therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1982

Anticonvulsant drugs determined by EMIT in spiked brain samples: a correlation with HPLC values.

Phenobarbital (PB), diphenylhydantoin (PHT) and carbamazepine (CBZ) levels were determined in spiked rat brain homogenates by means of the EMIT assay, and these were compared with results obtained by high-pressure liquid chromatography (HPLC). The extraction procedure of the three drugs was identical for both methods, with minor modifications for EMIT (no addition of internal standard; reconstitution with the buffer used in routine plasma level analysis). Correlation coefficients between the data obtained by EMIT and HPLC were extremely good (PB, 0.90-0.98; PHT, 0.92-0.98; CBZ, 0.93-0.99). The results indicate that the EMIT system can detect PB, PHT, and CBZ in brain tissue with good accuracy, although HPLC remains the most accurate and proven method available for research purposes.

Animals↗
PubMed1980

Polypeptide synthesis catalyzed by p-hydroxymercuribenzoate-modified ribosomes.

The stimulation of poly(U)-directed polyphenylalanine synthesis produced by modification of Escherichia coli ribosomes with p-hydroxymercuribenzoate, at low molar ratios of reagent to ribosomes, is due to an increase in the average chain length of polyphenylalanine synthesized, and not to the activation of inactive ribosomes. At a higher molar ratio of p-hydroxymercuribenzoate to ribosomes, which produces no overall change in activity, approximately 50% of the active ribosomes present in the untreated preparation have been completely inactivated, and the remaining active ones, like the ribosomes of the stimulated preparation, synthesize polyphenylalanine at an increased rate as compared with the untreated ribosomes.

Dose-Response Relationship, Drug↗
PubMed1978

Structure of the yeast ribosomes. Proteins associated with the rRNA.

Polyamines have been shown to bind to doubled stranded regions of rRNA [3]. Therefore, ribosomal proteins that can be cross linked to these molecules in the ribosomes structure must be bound to or located in the vicinity of the RNA. This technique is the first to yield results on the proteins associated with the rRNA in the eukaryotic ribosome where the lack of purified ribosomal proteins does not allow the use of direct binding studies as in bacterial systems. Proteins S7, S10, S13, S21, S22 and S27 in the small subunit and L2/3, L5, L10/12, L19/20, L22, L23, L36/37, L42 and L43' in the large subunit are labelled when cross linked to [14C]spermidine using 1,5-difluoro 2,4-dinitrobenzene and are good candidates to be RNA-binding proteins in ribosomes from Saccharomyces cerevisiae.

Molecular Weight↗
PubMed1978

Proteins associated with rRNA in the Escherichia coli ribosome.

Ribosomal proteins located near the rRNA have been identified by cross linking to [14C]spermine with 1,5-difluoro-2,4-dinitrobenzene. The polyamine binds to double-stranded rRNA; those proteins showing radioactivity covalently bound after treatment with the bifunctional reagent should therefore be located in the vicinity of these regions of rRNA. Six proteins from the small subunit, S4, S5, S9, S18, S19 and S20 and ten proteins from the large subunit L2, L6, L13, L14, L16, L17, L18, L19, L22 and L27 preferentially take up the label. The results obtained with three proteins from the large subunit, L6, L16 and L27, show a high degree of variability that could reflect differences of conformation in the subunit population. Several proteins were drastically modified by the cross-linking agent but were not detected in the two-dimensional gel electrophoresis (e.g., S1, S11, S21, L7, L8 and L12) and therefore could not be studied.

Dinitrofluorobenzene↗
PubMed1978

Binding of [3H]narciclasine to eukaryotic ribosomes. A study on a structure-activity relationship.

[3H]Narciclasine is a specific inhibitor of peptide bond formation on eukaryotic ribosomes and binds to 60-S ribosomal subunits. Binding of [3H]-narciclasine to yeast ribosomes is inhibited by many other inhibitors of peptide bond formation including anisomycin, several sequiterpene antibiotics (trichodermin, trichothecin, fusarenon X and verrucarin A) several Cephalotaxus alkaloids (harringtonine, homoharringtonine and isoharringtonine), several Amaryllidaceae alkaloids (pretazettine, haemanthamine, lycorine, pseudolycorine and dihydrolycorine) and the narciclasine derivatives trans-dihydronarciclasine, trans-dihydronarciclasine acetonide and isonarciclasine. Binding is also inhibited, although to a very small extent, by methylnarciclasine and cisdihydronarciclasine. In contrast, no inhibition of [3H]narciclasine binding was observed in the presence of certain other inhibitors of peptide bond formation including blasticidin S, gougerotin, sparsomycin and puromycin.

Alkaloids↗
PubMed1978

Inhibition, by selected antibiotics, of protein synthesis in cells growing in tissue cultures.

A large number of compounds including actinobolin, adrenochrome, amicetin, anisomycin, aurintricarboxylic acid, blasticidin S, chartreusin, chlortetracycline, cycloheximide, doxycycline, edeine A1, edeine complex, emetine, fusidic acid, gougerotin, GppCH2p, oxytetracycline, pactamycin, polydextran sulphate, puromycin, pyrocatechol violet, sparsomycin and tubulosine have been tested for inhibitory effects on protein synthesis in cultured cells from both mouse fibroblasts (3T6 cells) and chick embryo fibroblasts (CEF). Essentially, similar results were obtained with both cell types with the most effective inhibitors being pactamycin, emetine, tubulosine, anisomycin and cycloheximide and with no significant inhibitory activity being detected with edeine complex, edeine A1, GppCH2p, polydextran sulphate, aurintricarboxylic acid, pyrocatechol violet and adrenochrome. The concentration of pactamycin required to produce 50% inhibition of protein synthesis approximated 5 X 10(-9) M, but for most of the inhibitors it ranged from 5 X 10(-6) M to 5 X 10(4) M. The molecular basis underlying these differences may be related, in addition to their intrinsic inhibitory power, to differences in permeability of the cells towards the various drugs tested. Alternatively, active accumulation of the drugs by the cells may be the variable parameter.

Animals↗
PubMed1976

Competition between trichodermin and several other sesquiterpene antibiotics for binding to their receptor site(s) on eukaryotic ribosomes.

1. Of the five sesquiterpene antibiotics tested and found to inhibit protein synthesis in yeast spheroplasts, trichothecin, trichodermol or trichodermin stabilized polyribosomes whereas, in contrast, verrucarin A or T-2 toxin induced 'run off' of polyribosomes with a corresponding increase in 80S monoribosomes. The effect of fusarenon X on the system could not be determined as the drug failed to enter the cells. 2. [acetyl-14C]Trichodermin bound to yeast polyribosomes with a dissociation constant of 2.10 muM and to yeast 'run off' ribosomes with a dissociation constant of 0.72 muM. 3. Trichothecin, trichodermol, fusarenon X, T-2 toxin and verrucarin A competed with [acetyl-14C]trichodermin for binding to its receptor site on 'run off' ribosomes. The observed competition was quantitatively similar for all drugs tested. In contrast, the five drugs competed to different extents with trichodermin for binding to its receptor site on polyribosomes. Thus trichothecin competed with relative efficiency, whereas verrucarin A competed poorly, and the other drugs occupied intermediate positions between these two extremes. 4. Studies were also carried out with yeast 'run off' ribosomes prepared from both a wild-type strain and a strain resistant to trichodermin. Competition experiments between verrucarin A and [3H]anisomycin indicated that verrucarin A bound to 'run off' ribosomes from the mutant strain less efficiently than to those from the wild-type.

Anisomycin↗