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Biomedical subjects

F Mora

Publications and source records attributed to F Mora.

At least 55 records · Page 3Linked to original sources
PubMed2000

[Outpatient care of upper gastrointestinal hemorrhage not related to portal hypertension].

BACKGROUND: The handling of upper gastrointestinal hemorrhage (UGH) usually includes the hospitalization of all patients, regardless of severity and prognosis. The aim of this paper is to assess the security of the outpatient control of some UGH, after their assessment in the hospital emergency room. PATIENTS AND METHODS: Prospective cohort of 533 patients who attended over 1994 and 1995 hospital emergency room for an episode of UGH not linked to portal hypertension. After clinical and endoscopical assessment in the emergency department, 422 cases (79%) were admitted and 111 (21%) discharged for outpatient care. An analysis is presented of the characteristics of both groups, their clinical outcomes and a multivariate analysis to assess the factors associated with the decision to admit the patient. RESULTS: Outpatients were young, with less comorbidity and better haemodynamic status than hospitalized patients. Most of outpatient cases UGH was due to gastroduodenitis, oesophagitis and Mallory-Weiss syndrome, as opposed to the greater importance of peptic ulcer in those admitted. All outpatients presented clean lesions or haematic remains. 25 (5.9%) hospitalized patients presented rebleeding, vs. only 1 (0.9%) outpatient (p < 0.05). When more severity cases were excluded from hospital group, the differences were not significant. All cases with active bleeding, severe haemodynamic repercussion or without endoscopy were admitted. For the remainder, the decision to admit was associated with the presence of bleeding stigmata, haemodynamic repercussion, some causes of hemorrhage, older age, and urea levels. CONCLUSIONS: Although the scarce sample do not permit definitive conclusions, results guide towards that a substantial part of UGH not linked to portal hypertension may be monitored without hospitalizing the patient, thereby minimizing care costs and increasing the productive capacity of the hospital, without increasing risks for the patient.

Ambulatory Care↗
PubMed1999

Therapeutic effects of different doses of botulinum toxin in chronic anal fissure.

PURPOSE: The aim of this study was to evaluate the clinical and manometric results of three different doses of botulinum toxin and two methods of injection for the treatment of chronic idiopathic anal fissure. METHODS: Sixty-nine patients with chronic anal fissure were included in a non-randomized, prospective trial of intrasphincteric injection of botulinum toxin. All patients reported postdefecatory anal pain lasting more than two months. Scoring systems were developed for anal pain, bleeding, and defecatory difficulty. Maximum resting and squeeze anal pressures were determined before and one month after treatment. Twenty-three patients undergoing a 5-U injection of diluted botulinum toxin A (BOTOX) on each side of the anal sphincter (total dose, 10 U) constituted the first group. In a second group 27 patients were injected as previously described, with an additional 5-U injection below the fissure (total dose, 15 U). The 19 patients constituting the third group received a 7-U injection on each side of the anus and below the fissure (total dose, 21 U). All patients were followed up for at least six months. RESULTS: Pain relief one month after treatment was more evident in the second and the third group (48 percent of patients in the first group, 74 percent in the second group, and 100 percent in the third group). A significant reduction of the mean resting pressure was demonstrated only in Groups II and III (P < 0.05), whereas the mean squeeze pressure significantly decreased in the three groups (P < 0.01 in Group I and P < 0.001 in Groups II and III). Fifty-two percent of the patients in the first group, 30 percent in the second group, and 37 percent in the third group were reinjected during the follow-up period, because of persistence of symptomatology or early relapse. The need for surgery was similar in the first and the second group (17 and 19 percent, respectively) and clearly lower in the last group (5 percent). No serious complications or incontinence attributable to this therapeutic modality developed in any patient. CONCLUSIONS: Intrasphincteric injection of botulinum toxin is a reliable new option in the treatment of uncomplicated chronic anal fissure. The healing rate is related to the dose and probably to the number of puncture sites. No permanent damage to the continence mechanism was detected in these patients.

Adult↗
PubMed1999

Amphetamine increases the extracellular concentration of glutamate in striatum of the awake rat: involvement of high affinity transporter mechanisms.

Using microdialysis it was found that intracerebral infusions of amphetamine increase the extracellular concentration of glutamate, and also of dopamine, aspartate, GABA, and taurine. The increases in glutamate produced by amphetamine was independent of calcium in the perfusion medium but was significantly attenuated by specific blockers of the high affinity transporters of this neurotransmitter. Amphetamine infusions also produced a decrease in the extracellular concentration of Na+, an increase in the extracellular concentration of lactate, and a decrease in haemoglobin in the area of perfusion. All these data suggest that amphetamine increases the extracellular concentration of glutamate and other neurotransmitters through a hypoxic mediated process. This study also shows that an alpha-noradrenergic receptor antagonist is able to attenuate the effects of amphetamine on the release of glutamate, dopamine, GABA and taurine, which further suggests a vasoconstrictor effect of amphetamine as a result of which hypoxia could develop.

ATP-Binding Cassette Transporters↗
PubMed1999

Endogenous GABA potentiates the potassium-induced release of dopamine in striatum of the freely moving rat: a microdialysis study.

Using microdialysis, a study was made of the effects of an increase of endogenous GABA on basal and potassium-stimulated release of dopamine in striatum of the awake rat. The dopamine metabolites DOPAC and HVA were also measured. Extracellular concentrations of GABA were increased by inhibiting its uptake with nipecotic acid. TTX (10 microM) reduced basal extracellular concentrations of dopamine, and dopamine metabolites, but not GABA. Nipecotic acid (200, 500, and 1000 microM) produced a dose-related increase in basal extracellular concentrations of GABA, but did not change basal extracellular concentrations of dopamine and dopamine metabolites. However, nipecotic acid significantly enhanced the dopamine release produced by perfusion of potassium (50 mM) and also enhanced the extracellular increase of GABA produced by high potassium. These results suggest that an increase of endogenous GABA is facilitating the stimulated release, but not the basal release, of dopamine in the striatum of the awake rat.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

Role of glutamate receptors and glutamate transporters in the regulation of the glutamate-glutamine cycle in the awake rat.

In the present study we investigate the effects of a specific glutamate reuptake blocker, L-trans-pyrrolidine-3,4-dicarboxylic acid (PDC), on extracellular concentrations of glutamine and glutamate in the striatum of the freely moving rat. Intracerebral infusions of PDC (1, 2 and 4 mM) produced a dose-related increase in extracellular concentrations of glutamate and a dose-related decrease in extracellular concentrations of glutamine. These increases in extracellular glutamate and decreases in extracellular glutamine were significantly correlated. To investigate the involvement of ionotropic glutamate receptors in the decreases of extracellular glutamine produced by PDC, N-methyl-D-aspartate (NMDA) receptor antagonist and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate receptor antagonist were used. Perfusion of the NMDA receptor antagonist blocked the decrease of extracellular glutamine but had no effect on the increase of extracellular glutamate, both produced by PDC. Perfusion of the AMPA/kainate receptor antagonist attenuated the increase of extracellular glutamate and not only blocked the decrease of extracellular glutamine but also produced a significant increase of extracellular glutamine. The results reported in this study suggest that both NMDA and AMPA/kainate glutamatergic receptors are involved in the regulation of extracellular glutamine.

ATP-Binding Cassette Transporters↗
PubMed1999

Endogenous dopamine increases extracellular concentrations of glutamate and GABA in striatum of the freely moving rat: involvement of D1 and D2 dopamine receptors.

Interactions between endogenous dopamine, glutamate, GABA, and taurine were investigated in striatum of the freely moving rat by using microdialysis. Intrastriatal infusions of the selective dopamine uptake inhibitor nomifensine (NMF) were used to increase the endogenous extracellular dopamine. NMF produced a dose-related increase in extracellular dopamine and also increased extracellular concentrations of glutamate, GABA, and taurine. Extracellular increases of dopamine were significantly correlated with extracellular increases of glutamate and GABA, but not taurine. To investigate whether the increased extracellular dopamine produced by NMF was responsible for the concomitant increase of glutamate and GABA, D1, and D2 receptor antagonists were used. Dopamine receptor antagonists D1 (SCH23390) and D2 (sulpiride) significantly attenuated the increases of glutamate and GABA produced by NMF. These data suggest that endogenous dopamine, through both D1 and D2 dopamine receptors, plays a role in releasing glutamate and GABA in striatum of the freely moving rat.

Animals↗
PubMed1999

Effects of endogenous glutamate on extracellular concentrations of GABA, dopamine, and dopamine metabolites in the prefrontal cortex of the freely moving rat: involvement of NMDA and AMPA/KA receptors.

Using microdialysis, interactions between endogenous glutamate, dopamine, and GABA were investigated in the medial prefrontal cortex of the freely moving rat. Interactions between glutamate and other neurotransmitters in the prefrontal cortex had already been studied using pharmacological agonists or antagonists of glutamate receptors. This research investigated whether glutamate itself, through the increase of its endogenous extracellular concentration, is able to modulate the extracellular concentrations of GABA and dopamine in the prefrontal cortex. Intracortical infusions of the selective glutamate uptake inhibitor L-trans-pyrrolidine-2,4-dicarboxylic acid (PDC) were used to increase the endogenous extracellular glutamate. PDC (0.5, 2, 8, 16 and 32 mM) produced a dose-related increase in dialysate glutamate in a range of 1-36 microM. At the dose of 16 mM, PDC increased dialysate glutamate from 1.25 to 28 microM. PDC also increased extracellular GABA and taurine, but not dopamine; and decreased extracellular concentrations of the dopamine metabolites DOPAC and HVA. NMDA and AMPA/KA receptor antagonists were used to investigate whether the increases of extracellular glutamate were responsible for the changes in the release of GABA, and dopamine metabolites. The NMDA antagonist had no effect on the increase of extracellular GABA, but blocked the decreases of extracellular DOPAC and HVA, produced by PDC. In contrast, the AMPA/KA antagonist blocked the increases of extracellular GABA without affecting the decreases of extracellular DOPAC and HVA produced by PDC. These results suggest that endogenous glutamate acts preferentially through NMDA receptors to decrease dopamine metabolism, and through AMPA/KA receptors to increase GABAergic activity in the medial prefrontal cortex of the awake rat.

Animals↗
PubMed1999

Multisensor fusion for atrial and ventricular activity detection in coronary care monitoring.

Information management for critical care monitoring is still a very difficult task. Medical staff is often overwhelmed by the amount of data provided by the increased number of specific monitoring devices and instrumentation, and the lack of an effective automated system. Specifically, a basic task such as arrhythmia detection still produce an important amount of undesirable alarms, due in part to the mechanistic approach of current monitoring systems. In this work, multisensor and multisource data fusion schemes to improve atrial and ventricular activity detection in critical care environments are presented. Applications of these schemes are quantitatively evaluated and compared with current methods, showing the potential advantages of data fusion techniques for event detection in noise corrupted signals.

Coronary Care Units↗
PubMed1999

Gastroesophageal reflux in diabetes mellitus.

OBJECTIVE: Although abnormal gastroesophageal (GE) reflux is the most frequent alteration of the gastrointestinal tract, its prevalence in diabetes mellitus (DM) is not widely known. The objective of this study was to analyze both the presence of abnormal GE reflux in diabetic patients with no esophageal symptoms and the influence of cardiovascular autonomic neuropathy (CVAN) in the development of abnormal GE reflux. METHODS: Fifty insulin-dependent diabetic patients, averaging 29.2 +/- 9.0 yr of age, who had had diabetes for > 5 yr and showed no symptoms or history of gastroesophageal disease, were compared with a control group composed of 36 healthy volunteers (18 men, 18 women) whose average age was 35.9 +/- 10.1 yr. The cardiovascular autonomic nervous system was examined in the diabetics and control subjects who complied with inclusion criteria. Long-term (24-h) ambulatory esophageal pH monitoring was performed, as well as a manometric study of the lower esophageal sphincter. RESULTS: The parameters obtained from the monitoring showed significant differences (p < 0.01) between DM and control subjects. Abnormal GE reflux, defined as any percentage of time with esophageal pH < 4 exceeding 3.5% of total time (8.7 +/- 5.6%; range, 4.1-24.4%), was detected in 14 patients. Diabetic subjects were classified according to cardiovascular autonomic neuropathy tests (without CVAN [n = 19, 38%] and with abnormal CVAN tests [n = 31, 62%]). The pH monitoring parameters showed significant differences between these two groups (p < 0.05). CONCLUSIONS: A higher prevalence (28%) of abnormal GE reflux appeared among asymptomatic diabetic patients than among the general population. The presence of abnormal GE reflux in diabetic patients was associated with the existence of cardiovascular autonomic neuropathy (abnormal GE reflux = 38.7% in diabetic patients with abnormal CVAN tests vs 10.5% in diabetic patients without CVAN).

Adult↗
PubMed1999

Etiological characterization of 512 severely mentally retarded institutionalized patients in havana.

OBJECTIVE: To investigate etiological factors in severe mental retardation (SMR). METHODS: An etiological study is presented of 512 SMR patients in five specialized institutions in Havana. RESULTS: Prenatal, perinatal and postnatal causes were apparent in 58.0, 24.8 and 11.1% of the patients, respectively; infantile psychosis was determined in only 0.4%. The remaining 5.6% were classified as having SMR of undeterminable origin, i.e. patients with apparently normal pre-, peri- and postnatal histories who had neither dysmorphism nor affected first-degree relatives, and had a normal karyotype and metabolic screen. Among prenatal causes, genetic factors were the most frequent (82.8%), while environmental factors were apparent in only 5.3% of these cases. Of the cases with prenatal genetic etiology, chromosomal aberrations were present in 86.5% (Down syndrome 96.2% and 3.7% other chromosomal aberrations), monogenic disorders in 11.3% [neurocutaneous diseases (32.1%) and fragile X syndrome (25%) were the most frequent], and multifactorial disorders in 2.0%. Thirty-five patients (11.7%) presented multiple congenital anomalies of 'prenatal unknown' causes. The latter group may include unidentifiable chromosomal aberrations, uniparental disomy, de novo mutations and multifactorial or teratogenic factors. CONCLUSION: Accurate determination of the etiology of SMR is important not only for genetic counseling purposes, but also in identifying prenatal events which make infants more vulnerable to perinatal risk factors.

Journal Article↗
PubMed1999

Effects of aging on the interaction between glutamate, dopamine, and GABA in striatum and nucleus accumbens of the awake rat.

The aim of the present study was to investigate, using microdialysis, the effects of aging on the glutamate/dopamine/GABA interaction in striatum and nucleus accumbens of the awake rat. For that, the effects of an increase of the endogenous concentration of glutamate on the extracellular concentration of dopamine and GABA in striatum and nucleus accumbens of young (2-4 months), middle-aged (12-14 months), aged (27-33 months), and very aged (37 months) male Wistar rats were studied. Endogenous extracellular glutamate was selectively increased by perfusing the glutamate uptake inhibitor L-trans-pyrrolidine-3,4-dicarboxylic acid (PDC) through the microdialysis probe. In young rats, PDC (1, 2, and 4 mM) produced a dose-related increase of dialysate concentrations of glutamate in both striatum and nucleus accumbens. PDC also increased dialysate dopamine and GABA in both structures. These increases were significantly correlated with the increases of glutamate but not with the PDC dose used, which strongly suggests that the increases of dopamine and GABA were produced by glutamate. In striatum, there were no significant differences in the dopamine/glutamate and GABA/glutamate correlations between young and aged rats. This means that the effects of glutamate on dopamine and GABA do not change during aging. On the contrary, in the nucleus accumbens of aged rats, the increases of dopamine, when correlated with the increases of glutamate, were significantly lower than in young rats. Moreover, the ratio of dopamine to glutamate increases at maximal increases of glutamate was negatively correlated with aging. On the contrary, the ratio of GABA to glutamate increases in nucleus accumbens was positively correlated with aging, which suggests that the effects of endogenous glutamate on GABA tend to be higher in the nucleus accumbens of aged rats. The findings of this study suggest that aging changes the interaction between endogenous glutamate, dopamine, and GABA in nucleus accumbens, but not in striatum, of the awake rat.

Aging↗
PubMed1999

[High resolution ECG signals in Chagas patients: SEARCH project].

This work presents contributions to the study of a public health problem known as Chagasic Myocarditis. The results of the efforts done in Venezuela to understand the evolution of this disease through a novel technique called High Resolution Electrocardiography (HRECG) are discussed. A review of this methodology is presented and also its potential as a tool to study Chagas disease and to diagnose its different myocardial manifestations is discussed in detail. Several research approaches are presented as well as the results obtained, new techniques for HRECG interpretation such as the analysis of signals from the P-R segment, the intra QRS potentials, and late potentials. This method contributes to early detection and follow up of Chagas myocarditis. The collection and the organization of a HRECG data base that served as the basis for SEARCH, which is a valuable resource for new research lines is also described.

Arrhythmias, Cardiac↗
PubMed1998

Amphetamine releases GABA in striatum of the freely moving rat: involvement of calcium and high affinity transporter mechanisms.

Using microdialysis the effect was investigated of amphetamine (AMPH) infusions into the striatum on the release of GABA in the freely moving rat. AMPH (5, 10 and 20 microg/microl), infused through a microdialysis probe at the rate of 2.5 microl/min, produced a dose-related increase in extracellular concentrations of GABA. At the highest dose (20 microg/microl), AMPH increased GABA from 0.08 +/- 0.01 to 0.67 +/- 0.14 microM. Increases in extracellular GABA produced by AMPH were both calcium-dependent and high affinity GABA transporter-mediated. A medium free of calcium reduced the increase of extracellular GABA produced by AMPH by 37%. Nipecotic acid (2, 4 and 8 mM), a specific GABA re-uptake blocker, significantly attenuated increases in extracellular GABA, but not GLU, produced by AMPH (20 microg/microl). This study is the first in vivo evidence showing the release of GABA produced by AMPH through a high affinity transporter mechanism.

Amphetamine↗
PubMed1998

Role of nitric oxide in modulating the release of dopamine, glutamate, and GABA in striatum of the freely moving rat.

This study investigated the role of nitric oxide (NO) in modulating the basal and N-methyl-D-aspartate (NMDA)-induced release of dopamine (DA), glutamate (GLU), and gamma-aminobutiric acid (GABA) in striatum of the freely moving rat using microdialysis. Intrastriatal infusion of NMDA (5 mM) for 15 min increased extracellular concentrations of DA, GLU, and GABA. NMDA also decreased extracellular concentrations of DA metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC), and 4-hydroxy-3-methoxyphenylacetic acid (HVA), and of the GLU and GABA precursor, glutamine (GLN). Perfusion of N-nitroarginine (1-5 mM), an inhibitor of the synthesis of NO, potentiated NMDA-induced increases in extracellular concentrations of DA and attenuated increases of extracellular GLU. NMDA-induced decreases of extracellular concentrations of DOPAC were also attenuated by N-nitroarginine. N-nitroarginine had no effect on NMDA-induced changes of extracellular concentrations of GABA, HVA, and GLN. N-nitroarginine decreased basal concentrations of DOPAC and HVA, and increase basal concentrations of GLN, but had no effect on basal DA, GLU, and GABA. These results suggest a role for NO in modulating the NMDA-induced release of DA and GLU in striatum. They also suggest that NO could be regulating the basal metabolism of DA, GLU, and GABA.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Amphetamine increases extracellular concentrations of glutamate in the prefrontal cortex of the awake rat: a microdialysis study.

Using microdialysis, the effect was investigated of intracerebral infusions of different doses of amphetamine (1.25, 2.5, 5, 10, and 20 microg/microl) on the extracellular concentrations of glutamate in the medial prefrontal cortex of the rat. Amphetamine produced a dose-related increase in extracellular concentrations of glutamate. At the highest dose, amphetamine increased extracellular glutamate by 445% of baseline as well as extracellular concentrations of taurine, and reduced extracellular concentrations of glutamine. Amphetamine did not modify other amino acids such as arginine. Increases in extracellular concentrations of glutamate and taurine were independent of calcium in the perfusion medium. This is the first study showing that amphetamine produces a calcium-independent increase in extracellular concentrations of glutamate and taurine in the medial prefrontal cortex of the rat.

Amphetamine↗
PubMed1998

Barrett's esophagus, markers to distinguish risk groups.

BACKGROUND: As compared to the general population, patients with Barrett's esophagus (BE) present a 30 to 40 times higher risk of developing cancer. Their prognosis is poor and it will only be changed trying to recognize and detect preneoplastic changes early in order to provide these patients with an effective surgical therapy. Although epithelial dysplasia is still the "gold standard" as a marker of increased risk for malignancy, in view of the inter and intraobserver differences for interpreting it, both as regards its existence and grade, we have investigated other markers which can show this increased cancer risk. OBJECTIVE: Our aim has been to analyze which parameters, in addition to dysplasia, can distinguish groups with a higher or lower risk of progression to malignancy for a differentiated follow-up, so that the cost-benefit ratio is adequate and a sufficiently early diagnosis can be achieved which allows for a healing surgical therapy in most patients. PATIENTS AND METHODS: Twenty-seven patients have been studied, 9 with BE without dysplasia (control group), 9 with Barrett's esophagus with dysplasia, and 9 adenocarcinomas over BE, in all of which the presence of p53, c-erb-2, PCNA and CEA was established by histochemistry and the existence of aneuploidy by static cytometry. RESULTS: PCNA was positive in the three groups, though it was not at the surface epithelium in 55.5% of the control cases. C-erb-2 was negative in all control cases and positive in 5 cases with dysplasia, and 2 with adenocarcinoma. Protein p53 was positive in one control case, in 2 with dysplasia, and 4 with adenocarcinoma. CEA was positive in 7 control cases and in all cases with dysplasia and adenocarcinoma. Finally, aneuploidy was found by static cytometry in 5 of 9 control cases, in 4 of 9 with dysplasia, and in all adenocarcinomas. From the analysis of the results obtained, it can be concluded that a positive marker, even in the absence of dysplasia, suggests the presence of a "genomic instability" which may lead to progression to malignancy. CONCLUSIONS: This study allows us to establish three risk groups (high, low and intermediate) for a differentiated follow-up which allows an early diagnosis, with an adequate cost-benefit ratio.

Barrett Esophagus↗
PubMed1997

Dopamine-glutamate interactions in the prefrontal cortex of the conscious rat: studies on ageing.

The effects of apomorphine, a D1-D2 dopamine receptor agonist, on the extracellular concentration of glutamate were investigated in the medial prefrontal cortex of young, middle-aged and aged rats. In vivo intracerebral perfusions were undertaken in the conscious rat using a concentric push-pull cannula system. Glutamate concentration in the samples were determined by HPLC with fluorometric detection. Apomorphine produced an increase in extracellular concentration of glutamate in medial prefrontal cortex of young rats (178% of baseline) only at 10 microM, but not at 5 and 20 microM. This increase in glutamate concentration induced by apomorphine was significantly attenuated by blockade of D1-D2 dopamine receptors with haloperidol. Apomorphine, at 10 microM, failed to induce an increase in extracellular concentration of glutamate in the prefrontal cortex of middle-aged and aged rats. However, at 20 microM, apomorphine induced an increase in glutamate concentration in the prefrontal cortex of middle-aged rats, but not in aged rats. These data indicate that an interaction between dopamine and glutamate exists in the medial prefrontal cortex and that this interaction deteriorates with age.

Aging↗