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Biomedical subjects

R Garrido

Publications and source records attributed to R Garrido.

At least 19 recordsLinked to original sources
PubMed2006

Stable neurovisual servoing for robot manipulators.

In this paper, we propose a stable neurovisual servoing algorithm for set-point control of planar robot manipulators in a fixed-camera configuration an show that all the closed-loop signals are uniformly ultimately bounded (UUB) and converge exponentially to a small compact set. We assume that the gravity term and Jacobian matrix are unknown. Radial basis function neural networks (RBFNNs) with online real-time learning are proposed for compensating both gravitational forces and errors in the robot Jacobian matrix. The learning rule for updating the neural network weights, similar to a back propagation algorithm, is obtained from a Lyapunov stability analysis. Experimental results on a two degrees of freedom manipulator are presented to evaluate the proposed controller.

Algorithms↗
PubMed2003

The role of the cytoskeleton in capacitative calcium entry in myenteric glia.

Capacitative calcium entry (CCE) is the process by which intracellular calcium is replenished from the external milieu upon depletion of intracellular stores. CCE is thought to participate in chemotaxis, proliferation and cell signalling. A physical interaction between intracellular stores and the plasma membrane is postulated to regulate CCE. We hypothesized that cytoskeletal disruption alters this interaction, inhibiting CCE in enteric glia. Cultured myenteric glia from neonatal guinea-pigs were treated with cytochalasin D (10 micro mol L-1), a microfilament disrupting agent, nocodazole (20 micro mol L-1), a microtubule disrupting agent, or vehicle (dimethyl sulphoxide). Intracellular calcium changes were measured using fura-2 microfluorimetry. To evaluate the rate of cation re-entry, barium was substituted for calcium because barium is not sequestered internally. Cytochalasin D-treated glia had diminished CCE responses (57 +/- 3 nmol L-1) compared with controls (97 +/- 7 nmol L-1) as did nocodazole-treated glia (30 +/- 2 nmol L-1) vs controls (77 +/- 6 nmol L-1). The proportion of cells demonstrating CCE abolition was greater in the cytochalasin (50 +/- 8%) and nocodazole-treated (89 +/- 2%) groups compared with controls (21 +/- 2%, 40 +/- 9%, respectively). Cytochalasin D and nocodazole treatment diminished the rate of cation re-entry based on diminished barium entry in treated vs control cells. From this study, we conclude that disruption of cytoskeletal elements diminishes calcium influx essential to calcium store repletion in myenteric glia.

Animals↗
PubMed2001

Nicotine protects against arachidonic-acid-induced caspase activation, cytochrome c release and apoptosis of cultured spinal cord neurons.

Hydrolysis of membrane phospholipids of spinal cord neurons is one of the first events initiated in spinal cord trauma. In this process, free fatty acids, and in particular arachidonic acid, are released. Exposure of spinal cord neurons to free arachidonic acid can compromise cell survival and initiate apoptotic cell death. In order to determine potential mechanisms of apoptosis induced by arachidonic acid, activation of caspases -3, -8, and -9, as well as the release of cytochrome c into the cytoplasm were measured in cultured spinal cord neurons exposed to 10 microM of this fatty acid. In addition, because nicotine can exert a variety of neuroprotective effects, we hypothesized that it can prevent arachidonic acid induced apoptosis of spinal cord neurons. To study this hypothesis, spinal cord neurons were pretreated with nicotine (10 microM for 2 h) before arachidonic acid exposure and caspase activation as well as markers of apoptotic cell death were studied. Treatment of spinal cord neurons with arachidonic acid for up to 24 h significantly increased cytoplasmic levels of cytochrome c, induced caspase activation and induced DNA laddering, a hallmark of apoptotic cell death. Nicotine pretreatment markedly attenuated all these effects. In addition, antagonist studies suggest that the alpha7 nicotinic receptor is primarily responsible for these anti-apoptotic effects of nicotine. These results indicate that nicotine can exert potent neuroprotective effects by inhibiting arachidonic acid induced apoptotic cascades of spinal cord neurons.

Animals↗
PubMed2001

Gastric intramucosal pH and intraluminal PCO2 during weaning from mechanical ventilation.

OBJECTIVE: To study the value of gastric intramucosal pH and gastric intraluminal PCO2 measurements to predict weaning outcome from mechanical ventilation. DESIGN: Prospective clinical study. SETTING: Intensive care medicine department of a university hospital. PATIENTS: Nineteen adult critically ill patients who were mechanically ventilated because of acute respiratory failure and were considered ready to be weaned. INTERVENTIONS: The patients were weaned with: synchronized intermittent mandatory ventilation plus positive end-expiratory pressure (SIMV+PEEP) or continuous positive airway pressure with pressure support ventilation (CPAP+PSV). A gastric tonometer was placed in all the patients. Tonometric, respiratory, and hemodynamic variables were measured during the weaning process. MEASUREMENTS: Hemodynamic variables, respiratory mechanics, pulmonary gas exchange, respiratory muscle force, spontaneous pattern of breathing, and the central control of breathing were recorded. Simultaneously, the intramucosal pH and gastric intraluminal PCO2 were measured. MAIN RESULTS: Eleven patients were successfully extubated and eight failed. The patients who failed showed higher values of mouth occlusion pressure, respiratory rate, and effective inspiratory impedance (mouth occlusion pressure/mean inspiratory flow). The intramucosal pH was initially 7.19 +/- 0.22 and decreased to 7.10 +/- 0.16 during the weaning process in patients who failed (p < .05). At the same time, the intramucosal pH showed a nonsignificant change from 7.36 +/- 0.07 to 7.32 +/- 0.07 in the patients who were successfully extubated. The intramucosal pH was statistically different when both groups were compared during the initial and the final evaluations (p < .05). For the initial evaluation, the sensitivity and specificity to predict weaning failure when the intramucosal pH was < or =7.30 were 0.88 (95% confidence interval [CI], 0.66-1) and 0.82 (95% CI, 0.59-1), respectively. The gastric intraluminal PCO2 was higher in patients who failed (p < .05). When gastric intraluminal PCO2 was . or =40 torr during the initial evaluation, weaning failure occurred with a sensitivity of 1 (95% CI, 0.31-1) and a specificity of 0.55 (95% CI, 0.26-0.84). CONCLUSIONS: Weaning failure was associated with gastric intramucosal acidosis. The intramucosal pH and gastric intraluminal PCO2 may be helpful to predict weaning outcome. Further controlled clinical trials in a larger group of patients are needed.

Adolescent↗
PubMed2001

Validity and reliability of the Portuguese version of the Confusion Assessment Method (CAM) for the detection of delirium in the elderly.

This study has tested the validity and reliability of the Portuguese version of the Confusion Assessment Method (CAM), a diagnostic assessment instrument for delirium developed by Inouye et al. (1990). The sample was formed by 100 patients with 60 and more years of age, admitted at the emergency service of Santa Casa de São Paulo, in the time periods between July and August, 1996, November and December, 1996 and February and March, 1997. The sensibility was 94.1% and specificity 96.4%. The assessors reliability in a sample of the 24 patients resulted in a kappa = 0.70. We have concluded that CAM is an adequate instrument to assess the presence of delirium, reliable to assess elderly patients at the emergency services.

Chi-Square Distribution↗
PubMed2001

[Microangiopathic hemolytic anemia and thrombocytopenia. Thrombotic thrombocytopenic purpura].

OBJECTIVE: Thrombotic thrombocytopenic purpura (TTP) or Moschovitz' syndrome is rare and is even rarer in childhood. Clinically, it is characterized by microangiopathic hemolytic anemia, thrombocytopenia, neurologic abnormalities, fever and renal dysfunction. The etiology is still unknown, although different factors such as large von Willebrand factor multimers and prostacyclin have been implicated. The acute form is more frequent, and in most cases the course is fulminant if treatment is not initiated. Laboratory data typically reveal hemolytic anemia, with schistocytes on the peripheral smear, diminished serum haptoglobin, and thrombocytopenia. MATERIAL AND METHODS: We present the clinical cases of two children, aged 4 and 7 respectively, with TTP, but with different evolution and treatment. Evolution was favorable in both patients. The first child recovered spontaneously. In the second plasmapheresis was required and produced remission of all the symptomatology. Normality has been maintained for 36 and 24 months respectively, and the children have presented no clinico-biological alterations.

Anemia, Hemolytic↗
PubMed2000

Nicotine attenuates arachidonic acid-induced neurotoxicity in cultured spinal cord neurons.

Arachidonic acid release from cellular membranes due to spinal cord trauma may be one of the principal destructive events that can lead to progressive injury to spinal cord tissue. Exposure to arachidonic acid can compromise neuronal survival and viability. Because nicotine is known to be a neuroprotective agent, we propose that it can prevent arachidonic acid-induced neurotoxicity. To study this hypothesis, effects of nicotine on mitochondrial function, cellular energy content and apoptotic cell death were measured in cultured spinal cord neurons treated with arachidonic acid. Nicotine attenuated arachidonic acid-induced compromised cell viability and cellular ATP levels in spinal cord neurons. Nicotine exerted these protective effects when used at the concentration of 10 microM and only after a 2-h pre-treatment before a co-exposure to arachidonic acid. Antagonists of nicotinic receptors, such as alpha-bungarotoxin or mecamylamine, only partially reversed these neuroprotective effects of nicotine. In addition, nicotine prevented arachidonic acid-induced activation of caspase-3 activity and apoptotic cell death. These results indicate that nicotine pre-treatment can exert a protective effect against arachidonic acid-induced injury to spinal cord neurons.

Adenosine Triphosphate↗
PubMed2000

Nicotine attenuates arachidonic acid-induced overexpression of nitric oxide synthase in cultured spinal cord neurons.

Primary spinal cord trauma can initiate a cascade of pathophysiologic events which markedly contribute to the expansion and amplification of the primary insult. The detailed mechanisms of these secondary neurochemical reactions are largely unknown; however, they involve membrane lipid derangements with the release of free fatty acids, in particular, arachidonic acid (AA). AA can induce several injury effects on spinal cord neurons. We hypothesize that upregulation of nitric oxide synthase (NOS) is among the most important mechanisms of arachidonic-acid-induced neuronal dysfunction and that nicotine can attenuate this effect. To study these hypotheses, spinal cord neurons were exposed to AA and/or nicotine, and several markers of neuronal nitric oxide synthase (nNOS) metabolism were measured. In addition, cotreatments with either inhibitors of nicotinic receptors or inhibitors of specific NOS isoforms were employed. Treatment with AA markedly increased activity of nNOS, as well as mRNA and protein levels of this enzyme. Changes in nNOS expression were accompanied by an increase in cellular cGMP and medium nitrite levels. Pretreatment with nicotine decreased AA-induced overexpression of nNOS and elevation of nitrite levels. In addition, it appeared that these nicotine effects could be partially modulated both by the alpha7 nicotinic receptors or by nonreceptor mechanisms. Alternatively, the observed changes could also be mediated by an alternate nicotinic receptor mechanism which is not blocked by alpha-bungarotoxin or mecamylamine. Results of the present study indicate that exposure to AA can lead to induction of nNOS in cultured spinal cord neurons. In addition, nicotine can exert a neuroprotective effect by attenuation of AA-induced upregulation of nNOS metabolism. These data may have therapeutic implications for the treatment of acute spinal cord trauma.

Animals↗
PubMed2000

Antagonistic oxytocin/alpha2-adrenoreceptor interactions in the nucleus tractus solitarii: relevance for central cardiovascular control.

The modulation of the central cardiovascular effects of alpha2-adrenoceptor activation by oxytocin in the nucleus tractus solitarii has been evaluated by cardiovascular analysis and by quantitative receptor autoradiography. Microinjections in the nucleus tractus solitarii of a threshold dose of oxytocin effectively and significantly counteracted the vasodepressor and bradycardic actions of an ED50 dose of the alpha2-adrenoceptor agonist clonidine. The coinjection of a threshold dose of oxytocin with a threshold dose of clonidine did not produce any changes in the mean arterial pressure but a tachycardic response was observed. Receptor autoradiographical experiments showed that oxytocin (3 nM) significantly increased the Kd and Bmax values of [3H]p-aminoclonidine binding sites in the nucleus tractus solitarii compatible with a possible antagonistic interaction with the alpha2-adrenoceptors, and this effect was blocked by the presence of the specific oxytocin receptor antagonist 1-deamino-2-D-Tyr-(OEt)-4-Thr-8-Orn-oxytocin. These findings suggest the existence of an antagonistic oxytocin/alpha2-adrenoceptor interaction in nucleus tractus solitarii that may be of relevance for the demonstrated modulation of alpha2-adrenoceptor induced cardiovascular responses by oxytocin.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2000

4-Hydroxynonenal induces oxidative stress and death of cultured spinal cord neurons.

Primary spinal cord trauma can trigger a cascade of secondary processes leading to delayed and amplified injury to spinal cord neurons. Release of fatty acids, in particular arachidonic acid, from cell membranes is believed to contribute significantly to these events. Mechanisms of fatty acid-induced injury to spinal cord neurons may include lipid peroxidation. One of the major biologically active products of arachidonic acid peroxidation is 4-hydroxynonenal (HNE). The levels of HNE-protein conjugates in cultured spinal cord neurons increased in a dose-dependent manner after a 24-h exposure to arachidonic acid. To study cellular effects of HNE, spinal cord neurons were treated with different doses of HNE, and cellular oxidative stress, intracellular calcium, and cell viability were determined. A 3-h exposure to 10 microM HNE caused approximately 80% increase in oxidative stress and 30% elevation of intracellular calcium. Exposure of spinal cord neurons to HNE caused a dramatic loss of cellular viability, indicated by a dose-dependent decrease in MTS [3-(4, 5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-s ulfophenyl)- 2H-tetrazolium, inner salt] conversion. The cytotoxic effect of HNE was diminished by pretreating neurons with ebselen or N-acetylcysteine. These data support the hypothesis that formation of HNE may be responsible, at least in part, for the cytotoxic effects of membrane-released arachidonic acid to spinal cord neurons.

Acetylcysteine↗
PubMed1999

Sleep complaints among the elderly: results from a survey in a psychogeriatric outpatient clinic in Brazil.

BACKGROUND: Sleep complaints are frequent in old age. These difficulties are often associated with health-related problems, drug consumption, and the presence of mental disorders. Nonetheless, only sparse information is available on the clinical characteristics of elderly persons with insomnia. AIMS: (a) To evaluate the prevalence of sleep problems among the elderly assessed in a psychogeriatric outpatient clinic; (b) to evaluate the association between the use of sleep tablets and sleep difficulties in this sample of patients. METHODS: One hundred eighteen consecutive subjects were recruited from a psychogeriatric outpatient service in São Paulo, Brazil. Their sleep pattern was systematically assessed with the "sleep inventory," a questionnaire consisting of 31 items that evaluate a number of sleep-related features. Clinical diagnoses followed the ICD-10 clinical descriptions and diagnostic guidelines. The number of drugs consumed by patients was also recorded. RESULTS: Sleep complaints were highly prevalent (59.3%), with early-morning awakening and nightmares being more frequent among patients with a depressive disorder. The use of sleep tablets was reported by 37.3% of subjects, and was associated with subjective sleep difficulties (odds ratio [OR] = 7.13, p = .008), difficulties falling asleep (OR = 7.33, p = .021), and frequent awakening during the night (OR = 7.10, p = .040) in a logistic regression analysis. CONCLUSION: Sleep dissatisfaction is frequent among psychogeriatric outpatients. Subjects taking hypnotic drugs have more sleep-related complaints than those who do not. The clinical use of hypnotics may not be very effective for the treatment of sleep-related problems in the elderly. There is an urgent need for systematic prospective controlled studies to assess the efficacy and safety of the various forms of treatment of insomnia in old age.

Aged↗
PubMed1999

Arachidonic acid-induced oxidative injury to cultured spinal cord neurons.

Spinal cord trauma can cause a marked release of free fatty acids, in particular, arachidonic acid (AA), from cell membranes. Free fatty acids, and AA by itself, may lead to secondary damage to spinal cord neurons. To study this hypothesis, cultured spinal cord neurons were exposed to increasing concentrations of AA (0.01-10 microM). AA-induced injury to spinal cord neurons was assessed by measurements of cellular oxidative stress, intracellular calcium levels, activation of nuclear factor-KB (NF-kappaB), and cell viability. AA treatment increased intracellular calcium concentrations and decreased cell viability. Oxidative stress increased significantly in neurons exposed to 1 and 10 microM AA. In addition, AA treatment activated NF-kappaB and decreased levels of the inhibitory subunit, IKB. It is interesting that manganese superoxide dismutase protein levels and levels of intracellular total glutathione increased in neurons exposed to this fatty acid for 24 h, consistent with a compensatory response to increased oxidative stress. These results strongly support the hypothesis that free fatty acids contribute to the tissue injury observed following spinal cord trauma.

Animals↗
PubMed1999

[Behavior problems in patients with dementia. The impact on the career life].

Many studies have suggested that caring for patients with dementia may be associated with increased burden, particularly when subjects present with prominent behavioural problems. The present work aimed to review studies appearing on MedLine between 1990 and January 1998 that included the following keywords: 'burden or impact or cost' and 'dementia or Alzheimer's disease' and 'carer or caregiver or caregiving or family'. Only fourteen of the studies retrieved fulfilled the entry criteria for this review: crossectional or longitudinal studies looking at the association between behavioural problems in patients with dementia and burden of carers. All studies indicated that behavioural disturbances are an important cause of burden, although there was little consistency on the definition of 'behavioural disturbances'. As a consequence, it is still unclear which behavioural symptoms are more closely associated with increased burden of care. Future research in the area should aim to clarify these issues and develop management strategies to decrease burden on carers of patients with dementia.

Aged↗
PubMed1996

[Systemic leptospirosis as a cause of multiple organ failure. Report of a case].

Leptospirosis is a world-spread zoonosis that is incidentally acquired by humans. It causes a diphasic febrile illness in which the Weil syndrome is its severest form, with renal, hepatic, clotting and central nervous system involvement. We report a 73 years old male, that was admitted to an intensive care unit with multiple organ failure due to leptospirosis. The clinical picture initially resembled a sepsis due to biliary tract obstruction and was operated, not finding a biliary tract obstruction. Considering the history of a fall to sewed waters, leptospirosis was suspected and treatment with penicillin was started, obtaining a full recovery of the patient.

Abdominal Pain↗
PubMed1989

YM461, a PAF antagonist, blocks antigen-induced late airway responses and airway hyperresponsiveness in allergic sheep.

We examined the effect of an orally active antagonist, YM461, of platelet activating factor (PAF) on antigen-induced early and late airway responses and on the development of airway hyperresponsiveness 24 h after challenge in allergic sheep. Early and late airway responses were determined by measuring specific lung resistance (SRL) before and periodically after challenge. Airway responsiveness was determined from the slopes of dose-response curves of SRL vs. increasing doses of carbachol aerosol. The sheep were challenged with Ascaris suum antigen once after vehicle treatment (control) and once 1 h after oral administration of 3 or 10 mg/kg YM461 (each trial was greater than or equal to 14 days apart). Airway responsiveness to carbachol was determined 1-3 days prior to and 24 h after antigen challenge. In control 1 and control 2 trials antigen challenge caused significant peak early (288 and 292%, respectively) and peak late (103 and 124%, respectively) increases over baseline in SRL. SRL returned to baseline 24 h after challenge but the sheep developed airway hyperresponsiveness as indicated by the 2.6-fold increases in the slopes of the carbachol dose-response curves in the control trials. YM461, 3 and 10 mg/kg p.o., significantly inhibited the late responses (66 and 82%, respectively) and blocked the development of airway hyperresponsiveness at 24 h. The early responses were not significantly reduced in either trial. These results suggest that PAF contributes to the antigen-induced late airway responses and associated airway hyperresponsiveness in allergic sheep.

Aerosols↗
PubMed1989

Effects of age and cigarette smoking on serum concentrations of lipids and apolipoproteins in a male military population.

The effects of age and cigarette smoking on lipids and apolipoproteins were studied in men, 20-65 years old, randomly selected from a military population in the Madrid area, Spain. Subjects were classified as non-smokers, medium smokers (10-20 cigarettes/day) and heavy smokers (more than 20 cigarettes/day). Smoking prevalence was 58%. Serum apolipoprotein A-I and HDL-cholesterol (HDL-C) were not age-dependent, while total cholesterol (TC), triglycerides (TG), LDL-cholesterol (LDL-C) and the TC/HDL-C ratio increased with age. None of the variables studied was age-dependent over 30 years. The effects of smoking on TC, TG, LDL-C, HDL-C, TC/HDL-C ratio, apolipoprotein A-I, apolipoprotein B, and apo A-I/apo B ratio in the 20-29-year-old group appeared to be prominent in heavy smokers (P values less than 0.001, less than 0.05, less than 0.01, less than 0.05, less than 0.001, less than 0.05, less than 0.01 and less than 0.05, respectively) but not in medium smokers, in which only TG increased significantly (P less than 0.001). Few differences were noted between non-smokers and smokers over 30 although the TC/HDL-C ratio did increase in heavy smokers (P less than 0.05).

Adult↗