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J Sabrià

Publications and source records attributed to J Sabrià.

13 recordsLinked to original sources

Distribution of alcohol dehydrogenase mRNA in the rat central nervous system. Consequences for brain ethanol and retinoid metabolism.

The localization of alcohol dehydrogenase (ADH) in brain regions would demonstrate active ethanol metabolism in brain during alcohol consumption, which would be a new basis to explain the effects of ethanol in the central nervous system. Tissue sections from several regions of adult rat brain were examined by in situ hybridization to detect the expression of genes encoding ADH1 and ADH4, enzymes highly active with ethanol and retinol. ADH1 mRNA was found in the granular and Purkinje cell layers of cerebellum, in the pyramidal and granule cells of the hippocampal formation and in some cell types of cerebral cortex. ADH4 expression was detected in the Purkinje cells, in the pyramidal and granule cells of the hippocampal formation and in the pyramidal cells of cerebral cortex. High levels of ADH1 and ADH4 mRNAs were detected in the CNS epithelial and vascular tissues: leptomeninges, choroid plexus, ependymocytes of ventricle walls, and endothelium of brain vessels. Histochemical methods detected ADH activity in rodent cerebellar slices, while Western-blot analysis showed ADH4 protein in homogenates from several brain regions. In consequence, small but significant levels of ethanol metabolism can take place in distinct areas of the CNS following alcohol consumption, which could be related to brain damage caused by a local accumulation of acetaldehyde. Moreover, the involvement of ADH in the synthesis of retinoic acid suggests a role for the enzyme in the regulation of adult brain functions. The impairment of retinol oxidation by competitive inhibition of ADH in the presence of ethanol may be an additional origin of CNS abnormalities caused by ethanol.

Alcohol Dehydrogenase↗

[Impact of a selective screening for gestational diabetes in a Spanish population].

BACKGROUND: Recently, the American Diabetes Association (ADA) concluded that pregnant women with low risk factors for gestational diabetes need not to be tested. The aims of this study was to determine the prevalence of gestational diabetes in a Spanish low risk pregnant women population, to analyze the criteria that define low risk pregnancies for gestational diabetes, and to compare the differences in morbidity between pregnant women with and without gestational diabetes. DESIGN AND METHODS: Cohort study of 2,262 gestations (2,085 Caucasians) during a period of 7 years in a reference hospital. RESULTS: The gestational diabetes prevalence was 15%. Two-hundred and seventy-four (12.1%) women were considered as a low risk group for gestational diabetes. Among these, 13 (4.7%) presented gestational diabetes in comparison with 16.6% in the remaining women (p = 0.0001). Gestational diabetes in the low risk pregnant women constituted the 3.8% of all gestational diabetes. We did not find differences in gestational outcomes or fetal antropometry between the groups. The relative risk of macrosomia in the low risk pregnant was 0.9% (95% confidence interval for the mean: 0.86-0.94). CONCLUSIONS: In spite of their capacity of identifying current complications, 4% of gestational diabetes would not have been diagnosed with the new ADA criteria. The misdiagnosis will prevent in this small group of women the adoption of preventive measures for subsequent pregnancies and for diabetes in later life.

Adult↗

Possible involvement of alpha 1-adrenoceptors in the modulation of [3H]noradrenaline release in rat brain cortical and hippocampal synaptosomes.

Nerve terminals obtained from rat brain cortex and hippocampus, were labelled with 0.04 microM of [3H]noradrenaline ([3H]NA). Thereafter the basal release of [3H]NA was measured in a Brandel superfusion apparatus, in the presence of alpha 1-adrenoceptor agonists (phenylephrine or noradrenaline) or these alpha 1-adrenoceptor agonists along with prazosin, an alpha 1-adrenoceptor antagonist. In cortical synaptosomes both alpha 1-adrenoceptor agonists increased the basal release of [3H]NA in a concentration-dependent manner (EC50 = 0.15 microM for phenylephrine and 12.6 microM for noradrenaline). Effects were reversed by 0.01 microM prazosin (EC50 = 2.46 and 130.1 microM, respectively). In synaptosomes from rat brain hippocampus, phenylephrine (EC50 = 1.28 microM) and noradrenaline (EC50 = 33.7 microM) also increased the [3H]NA release and prazosin (0.01 microM) shifted the corresponding concentration-response curves to the right (EC50 = 7.38 and 264.0 microM, respectively). Events produced by noradrenaline acting as alpha 1-adrenoceptor agonist did not show Ca2+ dependence. These results suggest (1) the presence of functional alpha 1-adrenoceptors in nerve terminals from rat brain cortex and hippocampus, (2) that these receptors seem to play a role in the presynaptic modulation of [3H]NA release, and (3) that intraterminal Ca2+ may be involved.

Adrenergic alpha-Agonists↗

A study of load cycling in a NiTi shape memory alloy with pseudoelastic behaviour used in dental prosthetic fixators.

NiTi alloy used in dental prosthetic fixators shows pseudoelastic behaviour and exhibits a great potential in dental and orthopaedic applications where constant correcting loads are required. In order to use such materials in dental prosthetic fixators, where the device is cyclically deformed, it is necessary to investigate the effect of the cyclic straining upon the transformation stresses and temperatures of the material. The aim of this work is to study the load cycling of a pseudoelastic NiTi shape memory alloy to be applied in the making of dental prosthetic fixators.

Biocompatible Materials↗

Relationship between serum IgE and airway responsiveness in adults with asthma.

BACKGROUND: General population studies have shown a relationship between total serum IgE levels and airway responsiveness, but this association has not been documented in patients with asthma. OBJECTIVE: The study assesses the cross-sectional relationship between IgE levels and airway responsiveness in 208 subjects who had had emergency department treatment for asthma at least 2 years earlier. METHODS: All participants completed a standardized respiratory questionnaire and underwent spirometry, allergy skin testing, and a dose-response methacholine challenge test. RESULTS: After adjusting for age and gender, the percentage of patients with asthma and airway responsiveness (provocative concentration causing a 20% fall in forced expiratory volume in 1 second [PC20] < or = 8 mg/ml) increased from 52% in the lower quintile of IgE to 72% in the upper quintile (p < 0.01). After adjusting for age, gender, baseline percent predicted forced expiratory volume in 1 second, and smoking, the association between IgE (both in quintiles and continuous) and PC20 appeared consistent and statistically significant (p < 0.01). This association was stronger in patients who were not given inhaled steroid (odds ratio for twice the concentration of IgE, 1.42; 95% confidence interval, 1.09 and 1.84), than in patients treated with inhaled steroid (odds ratio, 1.10; 95% confidence interval, 0.82 and 1.50). Eosinophilia and skin reactivity were associated with PC20 although to a lesser extent. CONCLUSION: These findings strengthen the role played by IgE in facilitating the development of bronchial responsiveness in patients with asthma.

Administration, Inhalation↗

Involvement of different types of voltage-sensitive calcium channels in the presynaptic regulation of noradrenaline release in rat brain cortex and hippocampus.

Transmitter release at the nerve terminal is mediated by the influx of Ca2+ through voltage-sensitive calcium channels (VSCCs). Many types of VSCCs have been found in neurons (T, N, L, and P), but uncertainty remains about which ones are involved in neuronal excitation-secretion coupling. Specific ligands for the L- and N-type VSCCs were used to determine which of these subtypes might be involved in the K(+)-evoked [3H]noradrenaline release from superfused rat brain cortical and hippocampal synaptosomes. In cortical presynaptic terminals the 1,4-dihydropyridine agonist Bay K8644 enhanced the K+ (15 mM)-evoked [3H]noradrenaline release. This effect was reversed by the 1,4-dihydropyridine antagonists nimodipine and nitrendipine. The L-type VSCC ligands had no effect on hippocampal synaptosomes. In contrast, the N-type VSCC blocker omega-conotoxin markedly reduced the K(+)-evoked [3H]noradrenaline release in nerve terminals from both regions. Inhibition was greater in hippocampal synaptosomes. When applied together the inhibitory actions of nimodipine and omega-conotoxin were approximately additive. These findings indicate that both L- and N-type VSCCs participate in noradrenaline release in rat brain cortex and suggest that noradrenergic terminals in the two regions examined may have distinct populations of VSCCs: L type in cortex and N type in hippocampus.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

A study of the abrasive resistance of metal alloys with applications in dental prosthetic fixators.

Wear is one of the main surface failure mechanisms in materials and it will play a leading role in substitutive dental biomaterials. The aim of the present study is to compare the abrasive wear of different metallic materials used in dental applications. The results show that the abrasive wear of alloys based on precious metals such as Pt, Pd, Au and Ag is higher than for Ti and Ti based alloys. The alloy with the highest wear resistance is the Co-Cr which exhibits as well the highest hardness and Young's modulus. Since the method corresponds to a well-established abrasive wear standard, the behaviour of the different materials can be easily compared.

Alloys↗

Clinical and functional characteristics of patients two years after being affected by the soybean asthma epidemic in Barcelona.

BACKGROUND: Patients affected during the asthma outbreaks caused by soybean dust inhalation in Barcelona presented with sudden onset of severe asthma followed by the rapid relief of symptoms after treatment. Two years after the epidemics ended, a case-control study was conducted in which the clinical, functional, and immunological characteristics of these asthma patients (a randomised sample of asthmatic patients admitted as emergency cases on epidemic days, n = 213) were compared with those of a control group (a random sample of asthmatic patients admitted as emergency cases for attacks of asthma on non-epidemic days, n = 170). METHODS: The study included the administration of the ATS-DLD78 standardised respiratory questionnaire, the measurement of atopy, and performance of spirometric tests and a methacholine inhalation test. RESULTS: Patients with epidemic asthma reported fewer symptoms of asthma, had attended emergency departments less frequently during the previous year for acute attacks of asthma, were taking fewer inhaled corticosteroids at the time of the study, and attended medical follow up less frequently than did the patients with non-epidemic asthma. However, the cases and controls showed no differences in ventilatory capacity or reactivity to the methacholine bronchoprovocation test. CONCLUSIONS: Two years after the end of the soybean epidemics, people affected by epidemic asthma had a favourable prognosis. This finding contrasts with a higher risk of life threatening asthma and death during the epidemics. This paradox could be the result of a complex interaction between host and conditions of exposure.

Asthma↗

Preventing asthma epidemics due to soybeans by dust-control measures.

BACKGROUND: The inhalation of soybean dust released during the unloading of soybeans into a silo caused outbreaks of asthma in Barcelona, Spain. This study was designed to determine morbidity due to asthma and serum IgE reactivity before and after the installation of filters in the silo. METHODS: We measured soybean-allergen concentrations in 136 samples of air collected for 9 months before and 24 months after the installation of filters. We compared the number of days on which there was an unexpected increase in emergency room visits for asthma, the number of days on which the number of emergency room visits for asthma in one four-hour period was so high that it was unlikely to be due to chance, and the mean daily number of emergency room and intensive care unit admissions for asthma for a total of 60 months before and after filter installation. Serum IgE antibodies against soybean allergens were measured in 38 patients before and after filter installation. RESULTS: The concentration of airborne soybean allergens on days when soybeans were unloaded decreased from 324 to 25 U per cubic meter after the installation of filters (P < 0.001). The number of days on which there was an unusually large number of visits to the hospital for asthma and the number of days on which asthma was epidemic both decreased significantly (both P < 0.001), from 29 to 6 and from 18 to 0, respectively. The mean daily number of emergency room and intensive care unit admissions for asthma on days when soybeans were unloaded decreased from 8.3 to 5.4 and from 0.26 to 0.01, respectively (both P < 0.001). The mean serum IgE antibody concentrations in the 38 patients studied decreased from 2 Pharmacia reference units per milliliter to 1 (P < 0.001). CONCLUSIONS: Installing filters on silos to prevent airborne dissemination of allergenic soybean dust eliminates outbreaks of asthma caused by inhalation of the dust, thus supporting the idea that the avoidance of allergens helps prevent asthma.

Adolescent↗

Synaptosomal (Ca2+-Mg2+)-ATPASE activity modulation by cyclic AMP.

Dibutyryl cyclic AMP, in a concentration-dependent manner, increased synaptosomal (Ca2+-Mg2+)-ATPase activity, but in synaptic plasma membranes lacked any effect. The maximal enzyme activity in synaptosomes was increased by 38%, leaving unaltered the extrasynaptosomal Ca2+ concentration necessary to reach it. In the presence of 5 microM cyclic AMP, cyclic AMP-dependent protein kinase increased (30%) maximal (Ca2+-Mg2+)-ATPase activity in synaptic plasma membranes, but the apparent affinity for Ca2+ was not modified. This effect was partially inhibited (60%) by a cyclic AMP-dependent protein kinase inhibitor. The data suggest that synaptosomal (Ca2+-Mg2+)-ATPase activity is modulated by a cyclic AMP-dependent phosphorylation reaction.

Animals↗

[Compliance of antibiotic treatment in primary health care. Value of the personalized prescription].

A controlled clinical study was carried out in order to evaluate the efficacy of a personalized prescription as a measure to improve the fulfillment of a short course antibiotic treatment. 180 patients completed the study (96 in the active group and 88 in the control group) finding no differences in selected variables between the two groups. Evaluation of treatment fulfillment was performed with an interview and counting the pills, finding with this method that 57.94% of the patients fulfilled the treatment. Except for a higher incidence of adverse side effects in the control group (p less than 0.05) no other significant differences were found between the two groups. The interview showed a 37% sensibility and a 97% specificity, which was specially usefull in the detection of nonfulfillers. The correlation coefficient between both groups was 0.66 (p less than 0.001). Our results suggest that the personalized prescription does not improve the patient compliance achieved by a good verbal information in the short course antibiotic treatment.

Adult↗

Histamine stimulated synaptosomal Ca2+ uptake through activation of calcium channels.

Histamine stimulated Ca2+ uptake in synaptosomes was completely inhibited by the slow Ca2+ channel antagonists verapamil, cinnarizine and flunarizine, and slightly inhibited by nifedipine and diltiazem. Ca2+ uptake in synaptosomes depolarized or predepolarized with varying K+ concentrations was increased by histamine, in both conditions, until 30mM K+. At higher K+ concentrations histamine was not able to alter K+ effects in either conditions. 30mM K+ stimulated uptake of Ca2+ in the absence or presence of histamine was not inhibited by verapamil and diltiazem. However nifedipine slightly inhibited K+ and K+ +histamine effects. 3-Isobutyl-1-methyl-xanthine and dibutyryl cyclicAMP potentiated (10%) the uptake of Ca2+ in synaptosomes induced by histamine. Dibutyryl cyclicAMP alone however decreased the basal Ca2+ uptake in a concentration-dependent manner. Verapamil, but not diltiazem, antagonized the effects elicited by 3-isobutyl-1-methyl-xanthine and dibutyryl cyclicAMP in the presence of histamine. The data suggest that the increase in synaptosomal Ca2+ uptake induced by histamine is mediated by the activation of the voltage sensitive calcium channels, and possibly a cyclicAMP-dependent protein kinase phosphorylation can modulate the opening of Ca2+ channels.

1-Methyl-3-isobutylxanthine↗