Biomedical subjects

C Arce

Publications and source records attributed to C Arce.

At least 19 recordsLinked to original sources

PubMed2006

Within-subject reliability and inter-session stability of EEG power and coherent activity in women evaluated monthly over nine months.

OBJECTIVE: Quantitative EEG parameters during resting conditions are used as baseline in research on cognition and in serial-EEG recordings. Despite its increasing use in cognitive research and the numerous evidences of the existence of sex differences in EEG, EEG stability has been mainly investigated in men. Particularly, studies on stability of coherent activity are scarce. The aim of this study was to investigate within-subject reliability and inter-session stability of resting EEG over a nine-month period in women. METHODS: Within-subject reliability and inter-session stability were analyzed for absolute power and inter- and intrahemispheric coherent activity at central and posterior regions, once a month, in resting conditions, with eyes open and closed. RESULTS: Within-subject reliability was very high (r>0.89) for all subjects and EEG parameters. Inter-session stability was higher with eyes closed and for interhemispheric coherent activity, and poorer with eyes open especially in the alpha band. CONCLUSIONS: Present results indicate high reliability of the pattern of power and coherent activity of each individual woman during rest, and group stability of EEG activity with eyes closed at least over a nine-month period. SIGNIFICANCE: These results provide information on EEG stability in women over a long period.

Adolescent↗

PubMed2006

Mitochondrial involvement in nitric oxide-induced cellular death in cortical neurons in culture.

Nitric oxide (NO) is an unstable molecule with physiological and pathological properties. In brain, NO acts as a modulator of neurotransmission as well as a protector against neuronal death from several death stimuli. However, beside this protector effect, high NO concentrations produce neuronal death by a mechanism in which the caspase pathway is implicated. In this work, we demonstrate that in cortical neurons the NO toxicity is mediated by mitochondrial dysfunction. SNAP, an NO donor, induces apoptosis in these cells because it 1) increases the p53 and 2) induces cytochrome c release and activation of caspase-9 and caspase-3. SNAP also induces necrosis, through 1) breakdown of the mitochondrial membrane potential, 2) ATP decrease, 3) ROS formation, and 4) LDH and ATP release, indicative of oxidative stress and death by necrosis. To sum up, in cortical neurons, high NO concentrations produced cellular death by both an apoptotic and a necrotic mechanism in which the mitochondria are implicated.

Adenosine Triphosphate↗

PubMed2005

Cadmium induces reactive oxygen species generation and lipid peroxidation in cortical neurons in culture.

Cadmium is a toxic agent that it is also an environmental contaminant. Cadmium exposure may be implicated in some humans disorders related to hyperactivity and increased aggressiveness. This study presents data indicating that cadmium induces cellular death in cortical neurons in culture. This death could be mediated by an apoptotic and a necrotic mechanism. The apoptotic death may be mediated by oxidative stress with reactive oxygen species (ROS) formation which could be induced by mitochondrial membrane dysfunction since this cation produces: (a) depletion of mitochondrial membrane potential and (b) diminution of ATP levels with ATP release. Necrotic death could be mediated by lipid peroxidation induced by cadmium through an indirect mechanism (ROS formation). On the other hand, 40% of the cells survive cadmium action. This survival seems to be mediated by the ability of these cells to activate antioxidant defense systems, since cadmium reduced the intracellular glutathione levels and induced catalase and SOD activation in these cells.

Adenosine Triphosphate↗

PubMed2005

SNAP, a NO donor, induces cortical neuron death by a mechanism in which the caspase pathway is implicated.

In this paper, we present data which demonstrate that, in cortical neurons, SNAP induces loss in cell viability as evaluated by the XTT test. This cell death started at 250 microM SNAP when the treatment was performed in a serum-free medium and at 10 microM when the treatment was given in the presence of serum. This death was mediated, at least in part, by an apoptotic mechanism detected by flow cytometry and DNA fractionation. The highest SNAP concentrations induced a dual behavior on caspase-3 activity. Concentrations of 250 microM in the absence of serum and 10 microM to 300 microM in the presence of serum produced caspase-3 activation. This indicates that NO induces neuronal death by an apoptotic mechanism in which the caspase pathway is implicated. Higher SNAP concentrations (500 microM to 1 mM) diminished the caspase-3 activity to levels similar or even lower than control values. This profile was observed in the absence as well as in the presence of serum in the medium. The caspase-3 inhibition mediated by the highest SNAP concentrations did not imply NO cellular protection since the caspase-3 inhibition mediated by these SNAP concentrations neither correlated with cellular viability nor with cellular apoptosis. The possible mechanism of caspase-3 inhibition at the highest SNAP concentrations used is discussed.

Animals↗

PubMed2005

Secretory carcinoma of the breast containing the ETV6-NTRK3 fusion gene in a male: case report and review of the literature.

SUMMARY BACKGROUND: Secretory carcinoma (SC) of the breast is a rare and indolent tumor. Although originally described in children, it is now known to occur in adults of both sexes. Recently, the tumor was associated with the ETV6-NTRK3 gene translocation. CASE PRESENTATION: A 52-year-old male was diagnosed with secretory breast carcinoma and underwent a modified radical mastectomy. At 18 months the tumor recurred at the chest wall and the patient developed lung metastases. He was treated concurrently with radiation and chemotherapy without response. His tumor showed the ETV6-NTRK3 translocation as demonstrated by fluorescent in situ hybridization (FISH). CONCLUSION: SC is a rare slow-growing tumor best treated surgically. There are insufficient data to support the use of adjuvant radiation or chemotherapy. Its association with the ETV6-NTRK3 fusion gene gives some clues for the better understanding of this neoplasm and eventually, the development of specific therapies.

Journal Article↗

PubMed2005

SNAP, a NO donor, induces cellular protection only when cortical neurons are submitted to some aggression process.

Nitric oxide is a versatile molecule, which plays important physiological and pathological roles. Its protective and toxic actions have been already evidenced in several cell types. However, the protective effect in cortical neurons remains elusive. In this work, we demonstrate that the NO-donor SNAP may induce both neuroprotection and neurotoxicity in this sort of cells. The protective effect of NO was evidenced when cortical neurons were exposed to deleterious conditions, such as serum deprivation. Serum deprivation induces apoptotic cortical neuron death through a caspase-dependent mechanism. Under these conditions, SNAP was able to oppose cell death through both caspase-3 inhibition and/or increase of antiapoptotic protein levels (Bcl-2 and Bcl-x(L)). On the other hand, in a normally serum-supplemented medium, high dose of SNAP behaves as a neurotoxic agent, through a mechanism which involves caspase-3 activation.

Animals↗

PubMed2004

Expression and functional properties of group I metabotropic glutamate receptors in bovine chromaffin cells.

We demonstrate the presence and functional properties of Group I metabotropic glutamate receptors (mGluRs) expressed in chromaffin cells. Immunocytochemical techniques revealed that two mGluR subtypes (mGluR1alpha and mGluR5) are expressed in chromaffin cells, located in both the cytoplasmic membrane and the cytosol surrounding the nucleus. These mGluRs are functionally active on catecholamine (CA) secretion in chromaffin cells because both (1S, 3R)-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD) and the specific agonist of Group I mGluRs, (S)-3,5-dihydroxyphenylglycine (DHPG), were able to stimulate the release of CAs (adrenaline and noradrenaline) in a dose-response manner. These effects were specifically reversed by L-(+)-2-amino-3-phosphonopropionic acid (L-AP3), a selective antagonist of the Group I metabotropic glutamate receptors. t-ACPD induced an increase in CA secretion in both the presence and absence of extracellular calcium, the former effect being accompanied by cell membrane depolarization. Noradrenaline (NA) release was higher in the presence of extracellular calcium than in its absence, whereas adrenaline release was of the same order under both conditions. These results indicate that different subtypes of Group I mGluRs are present in noradrenergic and adrenergic cells. Fluorescence imaging techniques in single cells showed different t-ACPD-induced increases in intracellular calcium in different chromaffin cells: in chromaffin cells, 67% expressed functional metabotropic glutamate receptors and with nicotinic receptors, whereas the remaining 33% expressed only nicotinic receptors. In the absence of external calcium, only about 25% of cells responded to t-ACPD-increased intracellular calcium by increasing inositol 1,4,5-trisphosphate (IP(3)) concentration and subsequent calcium mobilization from intracellular stores, whereas the remaining 75% increased intracellular calcium by promoting Ca(2+) influx from the extracellular medium through L- and N- but not P/Q voltage-dependent calcium channels.

Adrenal Medulla↗

PubMed2002

Production and characterization of monoclonal antibodies against dog immunoglobulin isotypes.

A panel of six monoclonal antibodies (mAbs) recognizing antigenic determinants on canine immunoglobulin (Ig) heavy or light chains was produced and characterized. All monoclonals recognized the IgG(2) subclass, although only two were subclass-specific (CA3H1 and CA4F1). The CA3B8 mAb was found to be specific for an epitope on canine immunoglobulin G heavy chain, (IgG(1) and IgG(2) subclasses). Two mAbs (CA2E9 and CA5B2) reacted with an epitope on the heavy chain of canine IgG and IgM and another, CA4E7, bound to canine IgA, IgG and IgM isotypes; CA4E7 recognized an epitope on canine immunoglobulin light chain. CA4E7, CA4F1 and CA5B2 recognized an epitope in the Fab region. Three mAbs, CA3B8, CA4E7 and CA5B2, showed much lower reactivity with canine IgG by ELISA when IgG was periodate-treated, suggesting that they recognized a carbohydrate determinant. Cross-reactivity analysis of these mAbs with sera from horse, goat, cow, sheep, pig, cat, rabbit, hamster, rat, mouse and human indicated that two mAbs, CA3B8 and CA5B2, recognized a canine IgG-specific epitope; two others, CA3H1 and CA4E7, recognized an epitope also present in rabbit and sheep immunoglobulin respectively; and the remaining two (CA2E9 and CA4F1) recognized an epitope broadly present on the Igs of the species analyzed. This panel of antibodies will be a useful tool for future canine immunodiagnosis tests. With the exception of CA2E9, all mAbs were able to recognize plasma cells on paraffin-embedded tissues, and will thus be useful for immunohistochemical assays.

Animals↗

PubMed2002

Trypanosoma cruzi mitochondrial malate dehydrogenase triggers polyclonal B-cell activation.

It has been proposed that Trypanosoma cruzi, the aetiologic agent of Chagas' disease, produces mitogenic substances responsible for the polyclonal B-cell activation observed during the acute phase of the infection. Isolation and characterization of the molecules involved in the induction of polyclonal activation observed during infectious diseases have posed a great challenge for the immunologist over the last decade. In this work we report that a 33 kD protein obtained from an alkaline fraction of T. cruzi epimastigotes (FI) stimulates proliferation and promotes differentiation into antibody-secreting cells of normal murine B cells in a T-cell independent manner. By flow cytometry we also found that the 33 kDa protein induces an increase in the expression of MHC class II and B7.2 but not B7.1 molecules on the B-cell surface. Sequencing by mass spectrometry identified the T. cruzi 33 kD protein as hypothetical oxidoreductase, a member of the aldo/ketoreductase family. In this report we demonstrate that this protein is also present in the infective bloodstream trypomastigote form of the parasite and was identified as T. cruzi mitochondrial malate dehydrogenase (mMDH) by enzyme activity and by Western blotting using a specific mMDH polyclonal antiserum. The biologic relevance of mMDH-induced polyclonal activation concerning T. cruzi infection is discussed.

Animals↗

PubMed2001

Swine platelet antigens: section report.

A total of 14 antibodies were found to label resting and/or activated swine platelets. Six recognized CD previously characterized for swine (CD29, CD41/61 and CD46). One had been characterized for human cells (CD47). Two antibodies with CD14 and SLA class I specificity suggested by the donor as well as five blind antibodies were also positive on platelets. One antibody appeared to recognize the swine homologue to human CD47, and four remained unclustered.

Animals↗

PubMed2001

Paradoxical sleep is characterized by uncoupled gamma activity between frontal and perceptual cortical regions.

STUDY OBJECTIVES: Coherent activity of fast activity has been postulated to be a common language of the brain involved in the processing of information and in integration of spatially separated but temporally correlated stimuli into whole events. Any disruption affecting temporality would result in distortion of cognitive activity. Dreaming during paradoxical sleep (PS) shows cognitive alterations that mimic frontal lobe dysfunction. Decreased temporal coupling of EEG between frontal and perceptual regions was hypothesized. The main objective was to explore temporal relationships of fast activity among these regions. DESIGN: N/A. SETTING: N/A. PARTICIPANTS: 8 young adults. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Interhemispheric (INTERr) and intrahemispheric (INTRAr) EEG correlation spectra (1-50 Hz) were obtained for wakefulness, stage 2, stage 4, and PS during the second night spent at the laboratory. INTERr showed a significant overall increase during sleep in comparison to wakefulness, whereas INTRAr of fast activity (27-48 Hz) between frontal-perceptual regions (F-P, F-O, F-T, Fp-P, Fp-T) decreased exclusively during PS while INTRAr among perceptual regions (P-O, P-T, O-T) maintained wakefulness values. CONCLUSIONS: Present results demonstrate state- and frequency-dependent shifts on temporal coupling. The hypothesized decrease in correlation of fast activity between frontal and perceptual regions during PS was confirmed. This decrease of temporal coupling might underlie the loss of voluntary direction of thinking and congruence with social and temporal context and the lack of judgment and passive acceptance of bizarreness during PS dreaming. The wakefulness levels in correlation of fast activity among perceptual regions might explain perceptual acuity during PS dreaming.

Adult↗

PubMed2001

Expression of CD61 (beta3 integrin subunit) on canine cells.

A monoclonal antibody (JM2E5) specific for the integrin beta3 chain, or CD61 or GPIIIa subunit, has been employed to determine the expression of the canine homologue CD41/CD61 or CD51/CD61 complex on different canine cells in peripheral blood lymphocytes, monocytes, granulocytes, platelets, erythrocytes, lymph-node cells, spleen cells and breast tumour cells). The canine homologue CD41/CD61 or CD51/61 was present on peripheral blood lymphocytes, monocytes, granulocytes, breast tumour cells and spleen cells as well as on platelets and it was absent from erythrocytes and lymph-node cells. An antigen with components of molecular masses of 25/100/120 kDa (under reducing conditions) was immunoprecipitated from canine peripheral lymphocytes and platelets, but not from granulocytes or monocytes. Expression on canine lymphocytes of the canine homologue of the human beta3 integrin chain was unexpected, based on the expression pattern of this molecule in human tissue.

Animals↗

PubMed2001

Nicotinic receptors mediate the release of amino acid neurotransmitters in cultured cortical neurons.

Nicotine stimulation of cortical neurons obtained from gestation day 19 rats provoked a dose-dependent release of aspartate, glutamate, glycine and GABA, indicating a functional role for the nicotinic receptor in this model. This release was exclusively Ca2+-dependent (vesicular release) in the case of aspartate and dual Ca2+-dependent and Ca2+-independent) for glutamate, glycine and GABA. Nicotine also raised the membrane potential and the intracellular calcium concentration. These effects were specific, since they were reversed by hexamethonium, an antagonist of the nicotinic receptor. It was shown that L, N, and P/Q type Ca2+ channels are involved in nicotine-mediated Ca2+ entry into cortical neurons. Evaluation of the effects of nicotine on Ca2+ entry in isolated cells showed that 100% of the cells responded to nicotine, although the intensity of the response was variable: 63% of the neurons showed an increase in intracellular Ca(2+) of 152 +/- 5 grey levels, 25% of 88 +/- 12 grey levels and 12% of 48 +/- 1 grey levels. Tetrodotoxin, which blocks voltage-dependent Na(+) channels, completely reversed nicotine-induced Ca2+ entry into single cells. This suggests that the Ca2+ increment is mediated by opening of Ca2+ channels and not by the nicotinic receptor.

Animals↗

PubMed2000

EEG bands during wakefulness, slow-wave and paradoxical sleep as a result of principal component analysis in man.

Human electroencephalogram (EEG) has been divided in bands established by visual inspection that frequently do not correspond with EEG generators nor with functional meaning of EEG rhythms. Power spectra from wakefulness, stage 2, stage 4 and paradoxical sleep of 8 young adults were submitted to Principal Component Analyses to investigate which frequencies covaried together. Two identical eigenvectors were identified for stage 2 and stage 4: 1 to 8 Hz and 5 to 15 Hz (87.95 and 84.62 % of the total variance respectively). Two eigenvectors were extracted for PS: 1 to 9 Hz and 10 to 15 Hz (81.62% of the total variance). Three eigenvectors were obtained for W: with frequencies between 1 to 7 Hz, 7 to 11 Hz, and 12 to 15 Hz (78.32% of the total variance). Power for all frequencies showed significant differences among vigilance states. These results indicate that slow wave activity can oscillate at higher frequencies, up to 8 Hz, and that spindle oscillations have a wider range down to 5 Hz. No theta band was independently identified, suggesting either that delta and theta oscillations are two rhythms under the same global influence, or that the traditional division of theta band in the human cortical EEG is artificial. Alpha as a band was identified only during wakefulness. Principal component analysis upon spectral densities extracted broad bands different for each vigilance state and from traditional bands, consistent with functional significance of EEG and with frequencies of generators of rhythmic activity obtained in cellular studies in animals.

Adult↗

PubMed1999

Amplitude reduction in visual event-related potentials as a function of sleep deprivation.

Eight adult males were subjected to 40 hours of total sleep deprivation (TSD). Reaction time in a visual task and electroncephalographam (C3) were evaluated every 2 hours. One second of EEG before the stimuli was Fourier-transformed, and 750 ms after target and nontarget stimuli were averaged and visual event-related potentials (ERP) were obtained. Factorial analysis identified time windows that showed significant amplitude reduction and longer latencies with TSD: (1) 140 to 288 ms (P180-N242-P281); (2) 288 to 413 ms and 601 to 749 ms (N382; P718) and; (3) 531 to 601 ms (N500). Effect was strongest for N382 and P718, the amplitudes of which dropped to 20% of original size. The entire waveform recovered initial amplitudes and latencies after recovery sleep except for P718 latency. Waveforms within similar time intervals have been associated with attentional gating, sensory discrimination, target selection, uncertainty and decision processes. Amplitudes of the visual ERP were inversely correlated with hours of TSD, reaction time, and absolute power of the prestimulus EEG. Present results clearly show changes in fundamental neurophysiologic mechanisms as a result of TSD, indicating variability and reduction of the alertness mechanisms and changes in thalamocortical gating affecting attention, discrimination and decision-making.

Adult↗

PubMed1997

Effect of spatial ability and sex on inter- and intrahemispheric correlation of EEG activity.

Inter- and intrahemispheric correlation of the EEG activity at rest was computed in two groups of men and women, between 17 and 21 years old, with extreme degrees of spatial ability (SA) evaluated by the Spatial Relations Subtest of the Differential Aptitudes Test (DAT). Interhemispheric (INTERr) and intrahemispheric (INTRAr) EEG correlations were computed by means of Pearson product-moment coefficients for 5 EEG bands after digitally filtering with an FFT. Women showed significantly higher INTERr of alpha 1 between left and right centrals, lower INTRAr between right frontal and right central regions and lower INTRAr within the left than in the right hemisphere. High SA subjects showed lower INTERr between left and right frontal derivations and higher INTRAr between frontal and parietal and between central and parietal regions of both hemispheres. Sex interacted with SA in INTRAr of alpha between right frontal and right temporal regions with high SA women showing lower INTRAr than low SA women and than men. The present results indicate a different inter- and intrahemispheric functional organization in men and women and in subjects with high and low spatial ability.

Adolescent↗

PubMed1996

Inter and intrahemispheric EEG correlation as a function of sleep cycles.

1. Inter (INTERr) and intrahemispheric (INTRAr) EEG correlation were assessed in 8 young male adults during wakefulness (W) with eyes closed before going to sleep, and during stage 2 (S2), stage 4 (S4) and paradoxical sleep (PS) of the first three sleep cycles during the second night spent at the laboratory. 2. Pearson product-moment correlation were calculated between EEG signals of each pair of electrodes (C3, C4, F3, F4, T3, T4) for every 0.5 Hz from 1.5 to 15 Hz. 3. INTERr and INTRAr of 1.5-6.5 and 11-15 Hz were significantly higher during stage 2 and 4; INTERr of 1.5-6.5 Hz was also higher during PS in cycle 1 and 2, whereas INTERr and INTRAr of 7-10.5 Hz were lower than during wakefulness. 4. INTRAr of S2 and S4 approximated, whereas INTRAr oF PS moved away from W over successive sleep cycles. 5. These data show that cortical changes during sleep are also observed in functional differentiation between cortical sites. Inter and intrahemispheric differentiation is attenuated during stage 2 and 4 while during PS only interhemispheric differentiation is attenuated but intrahemispheric differentiation is accentuated compared to wakefulness. This pattern of cortical differentiation may be of relevance for the understanding of mental activity changes during sleep.

Adult↗

PubMed1996

Time course of reaction time and EEG while performing a vigilance task during total sleep deprivation.

Nine young adult male (23-30 years old) paid volunteers were subjected to total sleep deprivation (TSD), after two consecutive nights in the laboratory, for 40 hours (from 0800 hours on the first day to 2400 hours on the following day). Oral temperature (OT), reaction time (RT) in a visual vigilance task, and electroencephalogram (EEG; C3, C4, T3, and T4) while performing the task were recorded every 2 hours during TSD and after recovery sleep. One second of EEG, before target and non-target stimuli for every subject and condition was visually inspected, and artifact-free epochs were Fourier transformed. Absolute power (AP) was calculated for 4-20 Hz (full band) and for theta, alpha 1, alpha 2, and beta 1. Analyses of variance (ANOVAs), with TSD and time-of-day as factors, showed the following significant results. TSD induced an increase in RT and AP of the full band at C3 and C4, of all bands at C3, of theta at T3, and of beta 1 at T4 (p < 0.009 for all comparisons). No time-of-day effects nor interactions were found. OT was not affected by TSD. All variables returned to baseline values after recovery sleep. RT and EEG power showed a linear increase with accumulating hours of wakefulness. The increment in RT also correlated with the increase in EEG power. The results demonstrate that the increment in RT is associated with the increase in AP, particularly in the left central cortex; that the EEG may be used to identify sleepiness; and that EEG during task performance is more sensitive to TSD than during relaxed wakefulness.

Adult↗